> Disorders > Pathologic Function > Bone Necrosis

Bone Necrosis

Bone necrosis, also known as avascular necrosis, is a condition where the bone tissue dies due to a lack of blood supply.
This can lead to the collapse of the affected bone and surrounding joint damage.
Bone necrosis can be caused by various factors, including injury, corticosteroid use, alcohol abuse, and certain medical conditions.
Early diagnosis and treatment are crucial to prevent further bone and joint deterioration.
Effective management options may include medication, physical therapy, and in some cases, surgical intervention.
Understanding the underlying causes and optimal treatment approaches is essential for improving outcomes for individuals suffering from this debilitating condition.

Most cited protocols related to «Bone Necrosis»

Palatal Bone Healing and Necrosis Analysis

At the study end (2 weeks after oral bone denudation), the palates were removed and fixed in 10% formalin. The palatal bones were decalcified in 10% EDTA, embedded in paraffin, sectioned, stained for Masson's Trichrome and TRAP, and histomorphometrically analyzed. The area of interest (AOI) was defined as the bone area within 1.0 mm from the palatal bone surface between the M1 and GPC (Fig. 1C). Numbers of empty and non-empty osteocyte lacunae were counted in each AOI in trichrome-stained sections and their ratio determined. Osteocyte analyses were completed for the contralateral AOI where no surgery was performed. Osteoclast perimeter (#/mm) was determined in each AOI in TRAP-stained sections. In this study a portion of bone in which greater than or equal to 10 adjacent empty osteocyte lacunae was defined as necrotic bone since such bone is devital (20 (link)). Therefore, small areas with less than 10 neighboring empty osteocyte lacunae were not counted as necrotic bone. The size of necrotic bone area was histomorphometrically measured using Image-Pro Plus v4 and compared between HZA and VC. The expression of von Willebrand factor (vWF) and CD68 in the connective tissue next to the AOI were immunohistochemically analyzed to assess blood vessels and macrophages in wounds, respectively. Sections were deparaffinized and enzymatic epitope retrieval was performed in 0.05% trypsin. Nonspecific protein was blocked with 10% goat serum. Sections were incubated at 4°C overnight with a mouse monoclonal CD68 antibody (MAB1435, Millipore, Billerica, MA) and a rabbit polyclonal vWF antibody (ab6999, Abcam, Cambridge, MA). Endogenous peroxidase activity was blocked with 0.3% hydrogen peroxide. Goat anti-mouse IgG (AP340P, Millipore) and anti-rabbit IgG (AP307, Millipore) conjugated to horseradish peroxidase were used for secondary antibodies and proteins developed with DAB (Vector Laboratories, Burlingame, CA). Sections were counterstained with hematoxylin and mounted. Numbers of vWF+ blood vessels and CD68+ cells per mm² in the oral mucosa next to the AOI were histomorphometrically assessed and compared.

Yamashita J., Koi K., Yang D.Y, & McCauley L.K. (2010). Effect of Zoledronate on Oral Wound Healing in Rats. Clinical cancer research : an official journal of the American Association for Cancer Research, 17(6), 1405-1414.

Publication 2010

anti-IgG Antibodies Blood Vessel Bone Necrosis Bones Cells Cloning Vectors Connective Tissue Edetic Acid Enzymes Epitopes Factor VIII-Related Antigen Formalin Goat Hematoxylin Horseradish Peroxidase Immunoglobulins Macrophage Monoclonal Antibodies Mucosa, Mouth Mus Operative Surgical Procedures Osteoclasts Osteocytes Palate Paraffin Embedding Perimetry Peroxidase Peroxides Proteins Rabbits Serum Tritium Trypsin Wounds

Osteonecrosis Induced in Mice

Using data from the Mouse Phenome Database of the Jackson Laboratory, we screened 14 strains of mice in pilot experiments on the basis of their known constitutive phenotypes which might predispose to osteonecrosis: A/J, BALB/cJ, DBA/2J (higher platelet counts); AKR/J, C3H/HeJ (higher plasma fibrinogen); B6AF1/J, B6C3F1, BALB/cBy, C3HeB/FeJ, CB6F1/J, NMRI (higher body weight); BTBR-T+tf/tf (lower prothrombin time); and C57BL/6J, CeH/HeJ (lower bone mineral density). Various regimens of oral dexamethasone in the drinking water for up to 15 weeks, methylprednisolone by intraperitoneal injection, and high-fat diets were given to a total of 185 mice from both genders of 14 strains (129 of whom were evaluable at the scheduled time point for histologic examination after 3 to 12 weeks of glucocorticoid therapy), and all bones in the appendages were evaluated histologically. The entire skeleton was evaluated using standard x-ray techniques. Osteonecrosis was identified histologically in a few mice but not radiographically. Osteonecrosis was only observed in male BALB/cJ and C57BL/6J mice on low-folate diets given dexamethasone in the drinking water. In the few animals (only 8 of 129) where osteonecrosis was identified histologically, the only joints affected were distal femurs. Osteonecrosis was not observed in controls receiving water without dexamethasone.
To decrease glucocorticoid induced infections, sulfamethoxazole/trimethoprim (280 mg sulfamethoxazole and 56 mg trimethoprim per 450 mL drinking water, three days a week) and tetracycline (1000 mg/L, seven days a week) were added to the drinking water.27 (link),28 (link) The interindividual coefficient of variation in consumption of drinking water containing dexamethasone has been reported to have a coefficient of variation of ~ 20%.29 (link)
Remaining experiments employed male BALB/cJ mice on low-folate diets, antimicrobial prophylaxis, and dexamethasone (or saline control) in the drinking water. In these definitive experiments, we evaluated only the right and left stifle joints, only by histology. A confirmatory experiment was conducted in which twelve mice were assigned to the continuous dexamethasone treatment at 4 mg/L for the first week and 2 mg/L dexamethasone thereafter until week 12.

Yang L., Boyd K., Kaste S.C., Kamdem L.K., Rahija R.J, & Relling M.V. (2009). A Mouse Model for Glucocorticoid-Induced Osteonecrosis: Effect of a Steroid Holiday. Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 27(2), 169-175.

Publication 2009

Animals Body Weight Bone Density Bone Necrosis Bones Dexamethasone Diet Diet, High-Fat Femur Fibrinogen Folate Glucocorticoids Infection Injections, Intraperitoneal Joints Magnetic Resonance Imaging Males Methylprednisolone Mice, House Mice, Inbred C57BL Mice, Laboratory Microbicides Phenotype Plasma Platelet Counts, Blood Radiography Saline Solution Skeleton Stifle Strains Sulfamethoxazole Tetracycline Times, Prothrombin Treatment Protocols Trimethoprim Trimethoprim-Sulfamethoxazole Combination Water Consumption

Quantifying Osteonecrosis and Inflammation in Maxillary Bone

Bones were decalcified in Cal-Ex II Fixative/Decalcifier (Fisher Scientific, Pittsburgh, PA, USA) for 4 to 6 days or in 14.5% EDTA (pH 7.2) for 4 weeks. Samples then were embedded in paraffin, and 5-μm-thick coronal sections at the interproximal area between the first and second maxillary molars were made. Thus each section included a complete cross section through the entire maxilla, which allowed a side-by-side comparison of the bone, teeth, and soft tissues from the ligature (right) and nonligature (left) sites.
To quantify the area of osteonecrosis and periosteal thickness, hematoxylin and eosin (H&E)–stained slides were digitally scanned using the Aperio XT automated slide scanner and the Aperio ImageScope Version 10 software (Aperio Technologies, Inc., Vista, CA, USA). One author (SD) marked the area(s) of osteonecrosis, defined as loss of more than five contiguous osteocytes with confluent areas of empty lacunae, and the total area was calculated by the ImageScope software. The ruler tool in ImageScope was used to measure the greatest area of buccal periosteal thickness on both the ligature and nonligature sides. Numbers of empty and total osteocytic lacunae were counted manually on the digital whole-slide image over a 1-mm-long and 0.25-mm-wide area of bone (length and width measured with the ImageScope ruler tool) at the buccal alveolus adjacent to the D1 root.
Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining using the DeadEnd Colorimetric TUNEL System Kit (Promega, San Luis Obispo, CA, USA) was performed on the section adjacent to that used for the H&E stain. For TUNEL quantification, TUNEL⁺ osteocytes and total osteocytes were counted manually within 1 mm adjacent to osteonecrotic foci or (if osteonecrosis was not present) within a 1 mm along the buccal alveolar bone.
Using a standard brightfield microscope, areas of mucosa overlying the alveolar crest with the greatest inflammation were identified. The high-power (×40) field with the greatest numbers of inflammatory cells was selected, and the numbers of polymorphonuclear cells and lymphocytes were counted manually.
All histology and digital imaging were performed at the Translational Pathology Core Laboratory (TPCL) at UCLA.

Aghaloo T.L., Kang B., Sung E.C., Shoff M., Ronconi M., Gotcher J.E., Bezouglaia O., Dry S.M, & Tetradis S. (2011). Periodontal Disease and Bisphosphonates Induce Osteonecrosis of the Jaws in the Rat. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 26(8), 1871-1882.

Publication 2011

Bone Necrosis Bones Cheek Bone Colorimetry deoxyuridine triphosphate DNA Nucleotidylexotransferase Edetic Acid Eosin Fingers Fixatives Hematoxylin Inflammation Ligature Lymphocyte Maxilla Microscopy Molar Mucous Membrane Osteocytes Paraffin Embedding Periosteum Promega Protein Biosynthesis Ridge, Alveolar Tissues Tooth Tooth Root Tooth Socket Transferase

Histopathological Assessment of Osteonecrosis

After the pilot experiments involving multiple appendages (see above), tissue samples from definitive experiments were obtained from distal femur only. Bone samples were fixed in 10% neutral buffered formalin overnight, then decalcified in TBD-2 (Thermo Fisher Scientific, Waltham, MA). The specimens were processed routinely and embedded in paraffin. Tissue sections were cut at 4 microns, stained with hematoxylin and evaluated by light microscopy.
Tissue samples were analyzed in a blinded fashion by an experienced veterinary pathologist (KB). Osteonecrosis was defined as the presence of all three of the following criteria: empty lacunae, pyknotic nuclei of ghost osteocytes in the bone trabeculae, and necrosis of the adjacent marrow and stromal elements.8 (link),11 (link),34 (link) All mice that had at least one osteonecrotic lesion in a stifle joint were considered positive for osteonecrosis, whereas those with no osteonecrotic lesions were considered negative for osteonecrosis.

Publication 2009

Bone Necrosis Bones Cancellous Bone Cell Nucleus Femur Formalin Light Microscopy Marrow Mus Necrosis Osteocytes Paraffin Embedding Pathologists Red Cell Ghost Stifle Tissues

Longitudinal Evaluation of Bone Marrow Lesions and Cartilage

Two musculoskeletal radiologists, blinded to case–control status and clinical data, read the BMLs and cartilage status according to the Whole-Organ Magnetic Resonance Imaging Score (WORMS) method.16 (link) Baseline and follow-up MRIs were read paired and with the chronological order known to the readers. BMLs and cartilage were assessed simultaneously. BML size was scored from 0 to 3 based on the extent of regional involvement. BMLs were scored in each of the five subregions in the medial and lateral compartments and in four subregions of the patellofemoral compartments, for a total of 14 subregions. Cartilage signal and morphology were scored according to the WORMS system from 0 to 6 in the same 14 articular surface regions. In a modification of WORMS developed for longitudinal readings, a score of 0.5 for any of the BML or cartilage lesions was introduced to reflect a within-grade change (+0.5 reflecting progression for cartilage lesions, +0.5 or −0.5 reflecting within-grade enlargement or regression, respectively).
Any change of ≥0.5 was defined as cartilage loss and any increase or decrease of ≥0.5 as a change in BMLs. The weighted κ coefficients of inter-reader reliability for the readings of bone marrow lesions (comparing 0–3 scores in each subregion) and cartilage (comparing 0–6 scores in each subregion) were 0.64 and 0.77, respectively.
An additional validation exercise of BML and cartilage scoring for the 1.0 T images was performed by both readers in consensus for 53 knees that also had received a 1.5 T MRI with the same sequence protocol. The weighted κ coefficients of the reliability readings for cartilage and BML scoring were 0.74 and 0.71, respectively. Sensitivity of cartilage assessment using the 1.5 T readings as a reference standard was 85.2%, specificity was 89.1%. Sensitivity and specificity for BML assessment were 73.0% and 96.4%, respectively.
Knees that showed typical radiological signs of traumatic bone contusions, osteonecrosis, fracture or malignant bone infiltration were excluded from the analysis. However, of all analysed MRIs, only one knee showed a subacute tibial depression fracture at follow-up and was excluded.

Roemer F., Guermazi A., Javaid M., Lynch J., Niu J., Zhang Y., Felson D., Lewis C., Torner J, & Nevitt M. (2008). Change in MRI-detected subchondral bone marrow lesions is associated with cartilage loss: the MOST Study. A longitudinal multicentre study of knee osteoarthritis. Annals of the rheumatic diseases, 68(9), 1461-1465.

Publication 2008

Bone Marrow Bone Necrosis Bones Cartilage Contusions Disease Progression Fracture, Bone Hypersensitivity Hypertrophy Joints Knee Magnetic Resonance Imaging Radiography Radiologist Tibial Fractures

Most recents protocols related to «Bone Necrosis»

Shoulder Arthroplasty Outcomes Before and After COVID-19

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2023

Anesthesia Anesthesia, Conduction Arthroplasty BAD protein, human Bone Necrosis Degenerative Arthritides Diagnosis Elbow Ethics Committees, Research Fellowships Fracture, Bone General Anesthesia Immobilization Index, Body Mass Intraoperative Complications Operative Surgical Procedures Orthopedic Surgeons Outpatients Pain Pandemics Patient Discharge Patients Prosthesis Rheumatoid Arthritis Rotator Cuff Tear Arthropathy Satisfaction Second Look Surgery Shoulder Skin Surgeons Therapy, Physical Vertebra Visual Analog Pain Scale Youth

Osteonecrosis of the Jaw: Trends and Demographics

By May 2021, the FAERS database contained a total of 22,002,078 reported cases of ADRs. Our methods include a wide search of the FAERS database for cases of medication induced ONJ with a total number of cases being reviewed at 19,668. The search strategy was that within the FAERS database we specified a “Search by Reaction Term” and looked up “Osteonecrosis of jaw.” We then selected a time frame with the first time period being similar to that of the original study from April 1, 2010 to December 31, 2014 (labeled as “time period 1”) and the second time period being from April 1, 2015 to Jan 12, 2021 (labeled as “time period 2”). Time periods 1 and 2 contained 8,253 and 11,415 cases respectively. We then determined our inclusion criteria for both sets of data. In doing so, we excluded patients that did not have gender listed as part of the patient demographics (ie, gender labeled as “Not specified”). Secondly, we did not include cases for patients below the age of 18, as we were primarily evaluating adult data. Thirdly, since the FAERS database allows consumers, healthcare professionals, and non-specified individuals to report their findings, we only included those reported by healthcare professionals allowing for increased accuracy of reporting. Lastly, we excluded duplicate cases using previously utilized methods, a multistep review process [4 (link)]. This involved identifying common patient characteristics from the FAERS database including patient age, gender, weight, event date, location (by country), drug reactions. After identifying patients with the same common characteristics, it was assumed these were duplicate patient information and thus, the duplicates were removed. This inclusion criteria nearly reduced the number of cases by nearly 60%, resulting in 3,132 cases in time period 1 and 5,776 in time period 2. This breakdown can be seen as a flow chart representation in Fig. 1. The top 20 medications were identified and described for these two different time periods. An analysis was performed on the collective patient demographics of medication-induced ONJ reports as well as for the two timeline ranges. Specific information obtained for this review included patient age, patient gender, associated medications, and indication for medication use. Descriptive statistics for all categorical [N (%)] variables were determined on all patients’ demographic and clinical characteristics. This project was submitted for review through Advocate Health and was waived as this study was deemed non-human subject related research.Fig. 1

Illustrates a flow chart representation of our inclusion criteria when comparing time period 1 (2010–2014 data set) to time period 2 (2015–2021 data set)

Ahdi H.S., Wichelmann T.A., Pandravada S, & Ehrenpreis E.D. (2023). Medication-induced osteonecrosis of the jaw: a review of cases from the Food and Drug Administration Adverse Event Reporting System (FAERS). BMC Pharmacology & Toxicology, 24, 15.

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Publication 2023

A 078 Adult Bone Necrosis Catabolism Drug Reaction, Adverse Gender Health Care Professionals Homo sapiens Patients Pharmaceutical Preparations Reading Frames TimeLine Vision

Evaluating Geriatric Osteoarthritis Patients

We included geriatric patients who were over 65 years and who had moderate or severe OA (Kellgren-Lawrence grade III or IV [8 (link)]) in this study. We excluded patients with rheumatoid arthritis, osteonecrosis, post-traumatic OA, a history of a psychiatric disorder, and those who did not consent to inclusion in this study. We evaluated patient characteristics including age, sex, body mass index, smoking status, hypertension, diabetes, and cancer (Table 1). We included 73 patients in the final sample. Of these, 83.6% (n = 61) were female, and the average age was 73.6 years (range, 65–85).Table 1

Demographic for entire study population (N = 73)

Variables	N (%)
Sex
Female: male	61 (83.6): 12 (16.4)
Body mass index
Normal	11 (15.1)
Overweight	15 (20.5)
Obesity	47 (64.4)
Smoking status
Nonsmoker	61 (83.6)
Former smoker	8 (11.0)
Current smoker	4 (5.4)
Hypertension
+: -	44 (60.3): 29 (39.7)
Diabetes
+: -	21 (28.8): 52 (71.2)
Cancer
+: -	15 (20.5): 58 (79.5)
KL grade
III: IV	48 (65.8): 25 (34.2)
	Mean (range)
Age (years, range)	73.6 (65–85)
Mean range of motion (°, range)
Extension	−6.7 (−11.3–0)
Flexion	122 (86.3–138.4)
Mean varus deformity (°, range)	7.8 (1.4–14.3)

Jung K.H., Park J.H., Ahn J.W, & Park K.B. (2023). Surgery-related anxiety on geriatric patients undergoing total knee arthroplasty: a retrospective observational study. BMC Musculoskeletal Disorders, 24, 161.

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Publication 2023

Bone Necrosis Congenital Abnormality Diabetes Mellitus Females High Blood Pressures Index, Body Mass Malignant Neoplasms Mental Disorders Patients Rheumatoid Arthritis Woman

Decompression and Autologous Bone Marrow Therapy for Early-Stage Non-Traumatic ANFH

We conducted a single-center prospective analytical study in a private hospital in Iraq on 31 patients with early-stage (stages I to III) non-traumatic ANFH. Baseline demographic data included age, gender, etiological factors, and ANFH stage according to the Ficat and Arlet classification based on plain radiograph, MRI, and the location of the necrotic lesion in each hip. A prospective, randomized, open-label was conducted involving patients who were developing ANFH at Iraqi private hospital, Iraq, from January 31, 2021, to November 2022. The intervention group received decompression and autologous bone marrow concentration (n=31).
The stage of ANFH was determined based on the Association Research Circulation Osseous (ARCO) classification 1994 for early-stage osteonecrosis, as follows:

Stage 0: Normal plain radiograph, normal computed tomography (CT), normal magnetic resonance imaging (MRI) or scintigraphy;

Stage I: Normal plain radiograph with abnormal CT or MRI;

Stage II: Plain radiograph: trabecular bone changes without variations in subchondral bone; MRI: unusual and diagnostic appearance;

Stage III: Plain radiograph: a highlight on the signs of a subchondral fracture displaying the "crescent sign";

Stage IV: Radiographic manifestation of femoral head flattening;

Stage V: Plain radiograph reveals a sign of femoral head flattening in addition to osteoarthritic variations, including decreased joint space and acetabula alteration;

Stage VI: It appears that the entire joint is destroyed.

Yousif N.G., Al Kilabi A.E., Hatem K.K., Al-Albaseesee H.H., Al-Fatlawy W.A., Alhamadani M., Nöth U.A, & Altmimi A. (2023). Autologous hematopoietic bone marrow and concentrated growth factor transplantation combined with core decompression in patients with avascular necrosis of the femoral head. Journal of Medicine and Life, 16(1), 76-90.

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Publication 2023

Acetabulum Avascular Necrosis of Femur Head Bone Marrow Bone Necrosis Bones Cancellous Bone Decompression Diagnosis Femur Heads Fracture, Bone Gender Joints Necrosis Patients Radionuclide Imaging Tomography, X-Ray X-Ray Computed Tomography X-Rays, Diagnostic

Evaluating Zoledronic Acid Safety

Information on any ARs, laboratory tests, and other measurements, especially of renal function and serum calcium, was collected. In association with the use of ZOL, the following conditions were included as the known, important risks: predefined acute-phase reaction (APR: pyrexia, malaise, arthralgia, myalgia, nausea, vomiting, influenza-like illness, headache, diarrhea, bone pain, pain in an extremity, and acute-phase reaction as reported by the attending physician), renal function-related ARs, hypocalcaemia, osteonecrosis of the jaw, and atypical femoral fracture. Any events were classified according to MedDRA ver. 23.0.

Takada J., Sato S., Arai K., Kito Y., Oshita Y, & Saito K. (2023). Safety and effectiveness of once-yearly zoledronic acid in Japanese osteoporosis patients: three-year post-marketing surveillance. Journal of Bone and Mineral Metabolism, 41(2), 268-277.

Publication 2023

Acute-Phase Reaction Arthralgia Bone Necrosis Bones Calcium Diarrhea Femoral Fractures Fever Headache Hypocalcemia Kidney Myalgia Nausea Pain Physicians Serum Virus Vaccine, Influenza

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What are the different types of bone necrosis?

Bone necrosis can occur in different forms, including avascular necrosis (also known as osteonecrosis), which is the most common type. This is caused by a disruption in blood supply to the bone, leading to the death of bone tissue. Other types include post-traumatic necrosis, which is due to injury, and secondary necrosis, which can result from conditions like sickle cell disease or organ transplantation.

What are some of the common causes of bone necrosis?

Bone necrosis can be caused by a variety of factors, including injury, corticosteroid use, alcohol abuse, and certain medical conditions. Injury can disrupt the blood supply to the bone, leading to necrosis. Prolonged use of corticosteroids can also reduce blood flow and contribute to bone cell death. Excessive alcohol consumption has been linked to the development of bone necrosis as well. Underlying medical conditions like sickle cell disease, lupus, and organ transplantation can also increase the risk of bone necrosis.

How can PubCompare.ai help with bone necrosis research?

PubCompare.ai can assist with bone necrosis research in several ways. First, it allows researchers to screen protocol literature more efficiently, helping to identify the most effective protocols related to bone necrosis for their specific research goals. Second, the platform's AI-driven analysis can highlight key differences in protocol effectiveness, enabling researchers to choose the best option for reproducibility and accuracy. This can be particularly helpful in ensuring the validity and reliability of bone necrosis studies, which are crucial for advancing our understanding and treatment of this condition.

How can early diagnosis and treatment help with bone necrosis?

Early diagnosis and treatment are crucial for managing bone necrosis and preventing further bone and joint deterioration. When bone necrosis is detected early, treatment options like medication, physical therapy, and in some cases, surgical intervention can be implemented to preserve the affected bone and joint. This can help slow or even halt the progression of the condition, reducing the risk of complications such as bone collapse and joint damage. By addressing bone necrosis in its early stages, patients have a better chance of maintaining their mobility and quality of life.

What are some common treatment options for bone necrosis?

The treatemnt options for bone necrosis can vary depending on the underlying cause and the stage of the condition. Common treatment approaches include: 1. Medication: Anti-inflammatory drugs, bisphosphonates, and other medications may be used to reduce pain and slow the progression of bone necrosis. 2. Physical therapy: Exercises and other physical therapy interventions can help maintain range of motion, strength, and function in the affected joint. 3. Surgical intervention: In more advanced cases, surgical procedures like core decompression, bone grafting, or joint replacement may be necessary to address bone and joint damage.

How can PubCompare.ai help optimize bone necrosis research protocols?

PubCompare.ai can help optimize bone necrosis research protocols by leveraging AI to pinpoint critical insights. The platform's AI-driven analysis can highlight key differences in protocol effectiveness, enabling researchers to choose the best option for reproducibility and accuracy. This can be especially helpful in ensuring the validity and reliability of bone necrosis studies, which are crucial for advancing our understanding and treatment of this condition. By screening protocol literature more efficiently and identifying the most effective protocols, PubCompare.ai can assist researchers in designing and implementing bone necrosis studies that are more likely to yield meaningful and reliable results.

More about "Bone Necrosis"

Bone necrosis, also known as avascular necrosis (AVN) or osteonecrosis, is a debilitating condition where the bone tissue dies due to a lack of blood supply.
This can lead to the collapse of the affected bone and surrounding joint damage, often causing significant pain and impaired mobility.
The condition can be triggered by various factors, including traumatic injury, prolonged use of corticosteroids, alcohol abuse, and certain underlying medical conditions such as sickle cell disease, Gaucher's disease, and systemic lupus erythematosus.
Early diagnosis and appropriate management are crucial to prevent further bone and joint deterioration.
Diagnostic tools like magnetic resonance imaging (MRI) and bone scans can help identify the extent and stage of the necrosis.
Treatment options may involve a combination of medication, physical therapy, and in some cases, surgical intervention.
Medications like methylprednisolone, a synthetic corticosteroid, can help reduce inflammation and pain, while physical therapy can improve joint mobility and strength.
In advanced cases, surgical procedures such as core decompression, bone grafting, or joint replacement may be necessary to address the structural damage and alleviate symptoms.
Specialized equipment like the Accu-Cut SRM 200 Sakura microtomes and the Zeiss AxioIma or Axio Scope A1 microscopes can aid in the histological assessment and analysis of bone samples, while the Eclipse LV100 POL polarizing microscope can be used to study the birefringent properties of bone tissue.
Understanding the underlying causes, early intervention, and the use of appropriate tools and techniques are essential for improving outcomes for individuals suffering from this debilitating condition.
By incorporating these insights, researchers and clinicians can enhance the reproducibility and accuracy of their bone necrosis studies, ultimately leading to better treatment and management strategies for patients.