T2: focal brightness marrow edema. Bone scan. However, other studies have also shown no benefit of preventing collapse with bisphosphonates.
FHL contracture. Risk of femoral head collapse with osteonecrosis is based on the modified Kerboul combined necrotic angle. Previous Next. Upgrade to PEAK. QID: L 4 Question Complexity. Question Importance. L 2 Question Complexity.
A synovial fluid aspirate of the hip demonstrates QID: L 1 Question Complexity. Orthobullets was not involved in the editorial process and does not have the ability to alter the question. L 3 Question Complexity. Sort by. This is further supported by CT scan analysis of samples that were used for Raman mapping that revealed that the radio density represented as Hounsfield number associated with AVNFH was significantly lower than the values for the controls.
Importantly, as reported by others, the mean number of HU within each region is a surrogate for bone mineral density 59 and higher Hounsfield values are associated with tissues having higher density Micro-cracks are microscopic cracks with length in the range of 30—80 microns The presence of trabecular micro-cracks in necrotic bone suggest healing defects and has been suggested to result in secondary vascular impairment in the capillaries either by causing compression of non-elastic fat cells or rupture of small intra-trabecular vessels Defect in bone structure was further visualized using histopathology that revealed absence of osteocytes within the necrotic zones.
These could represent areas of dead bone as reported by others Despite these extensive changes in bone architecture, plasma levels of bone resorption markers like osteocalcin and parathyroid hormone PTH did not change in AVNFH patients compared to controls.
Our results corroborate with that of earlier reports where in osteocalcin and a set of bone formation and resorption markers did not vary significantly between Osteonecrosis of knee and control patients Intriguingly however, osteocalcin expression associated with osteoblasts in the sections of trabecular bones were significantly altered in AVNFH compared to controls. Interestingly, osteoblasts lining the bone in areas of necrosis or fracture repair where extensive bone remodelling is known to occur strongly stained for osteocalcin.
These results are in line with previous reports that show increased osteocalcin deposition in AVNFH areas In contrast, osteoblasts in healthy bone or in regions distal from sites of necrosis or bone repair showed weak osteocalcin expression.
Furthermore, CTX levels, an independent bone resorption marker showed a higher likelihood of being elevated in AVN compared to controls in a small pilot study that needs to be verified in larger patient and control cohorts. Importantly, these findings suggest that AVNFH is more likely a localized disease with active remodelling of the bone occurring in specific areas associated with necrosis. Our immunohistochemistry data also showed significant non-specific intense staining in the marrow potentially due to high levels of peroxidase activity in these tissues.
Yet another explanation for unchanged levels of bone resorption markers in the small group of AVNFH plasma that we analysed could be that these patients presented with advanced stage disease stage 3 and 4. Elevated levels of homocysteine and metabolites belonging to the homocysteine and polyamine pathway in the plasma are associated with Avascular Necrosis of the Femoral Head. The increase in homocysteine is correlated with a decrease in vitamin B 12 , B 6 and betaine.
Micro-Raman spectroscopy study shows that the bone from AVNFH patients displays decreased phosphate to amide and carbonate to amide ratio indicative of reduced mineralization.
Raman mapping interestingly revealed a significantly higher carbonate to phosphate ratio, indicative of bone resorption, as well as decreased mineral to matrix ratio indicative of decreased mineralization in AVNFH bones consistent with the CT scan data demonstrating reduced bone mineral density.
Consistent with all of this, SEM and histopathology reveal the presence of disrupted trabeculae and micro-cracks, co-existing with regions of dead bone as well as loss of osteocytes with associated necrosis of the marrow. Taken together, these data suggest extensive remodelling in AVNFH bones which is supported by increased expression of osteocalcin in osteoblasts associated with necrotic sites.
Informed consent was obtained from all subjects. Sections of trabecular bone or plasma from de-identified AVNFH patients were obtained from Sri Sathya Sai Institute of Higher Medical Sciences with approval from the institutional bioethics commission and patient consent. This included retrospective data from 55 patients and prospectively collected data from 14 patients currently consulting at the hospital.
For these parameters, missing values in patients or controls were computed using the median value for the entries in the corresponding experimental group i. The levels for each of the parameter were then visualized relative to the corresponding clinical reference range. To determine the significance in the altered levels of parameters in AVNFH relative to control, a student t-test was applied. Logistic regression model was built using all the variables including age and gender.
The predictive power for these three parameters was verified using a fold cross validation repeated times. Plasma was extracted from blood samples collected in EDTA coated tubes following standard protocols.
For extraction of metabolome, plasma samples were homogenized in ice cold water: methanol mixture containing equimolar mixture of 2 standard compounds, Zeatine, [15N] 2-Tryptophan. Extracts were de-proteinated by passing through a 3 KDa filter, filtrate was dried, resuspended in injection solvent water: acetonitrile, , containing 0. Multiple Raman spectra were obtained along the diameter of the bone slice at — micron intervals, by focusing the laser beam through a 50XLWD long working distance microscope objective.
For control specimen, an equivalent number of Raman spectra were obtained along the diameter of the bone slice. For each of the bone slices, a line scan typically comprising of 10—12 spots was carried out along the entire cross section of the bone.
The normalized data was used for downstream statistical analysis to compare and quantify the mineral-matrix components in the AVNFH bone versus the control bone like bone crystallinity, Carbonate to amide ratio and Phosphate to amide ratios. Laser beam was focused on the sample through 10X objective. The typical spot size impinging the sample was 3. A similar area was also chosen in the control bone samples for analysis.
Raman maps showing the intensities of phosphate, amide and carbonate functional moieties along with ratios for Carbonate to phosphate and mineral to matrix ratio were computed. Median values with associated standard deviations were used to compare between the groups. Two-sided t-test was used to determine the significance of the results. Notably, for the SEM analysis, the bone samples were not sputter coated so as to avoid any artifacts. CT acquisition was carried out in high resolution mode using the application software 13MW Multiple elliptical Regions of Interest ROI , each having an area of 50 mm 2 and perimeter size of 25 mm were superimposed on the reconstructed images of each of the bone slice using the synapse platform.
The sections were stained using Hematoxylin and Eosin and reviewed by two board certified bone pathologists from M. Prior to osteocalcin staining, tissues were de-paraffinized in xylene and rehydrated in graded alcohols. The antigen-antibody reaction was visualized after diaminobenzidine Sigma-Aldrich, MO and the slides were counterstained with hematoxylin Sigma-Aldrich, MO and mounted with Permount media.
Positive controls were stained in parallel; negative controls were generated by omitting the primary antibody. Experiments on humans and the use of human tissue samples. We confirm that all experiments were performed in accordance with relevant guidelines and regulations. Kamal, D. Epidemiologic study of avascular necrosis of the femoral head. Health Sci. Mont, M. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am 77 , — Chao, Y. Investigation of alcohol metabolizing enzyme genes in Chinese alcoholics with avascular necrosis of hip joint, pancreatitis and cirrhosis of the liver.
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Hemoglobin 25 , — Vitamin supplementation reduces the level of homocysteine in the urine of autistic children. This content does not have an Arabic version. Overview Avascular necrosis is the death of bone tissue due to a lack of blood supply. Request an Appointment at Mayo Clinic.
Share on: Facebook Twitter. Show references Jones LC, et al. Osteonecrosis avascular necrosis of bone. Accessed Feb. Avascular necrosis of the hip. Rochester, Minn. The goal of treatment is to improve functionality and stop further damage to the bone or joint. Treatments are needed to keep joints from breaking down, and may include:.
Core decompression. This procedure reshapes the bone and reduces stress on the affected area. Bone graft. In this procedure, healthy bone is transplanted from another part of the body into the affected area. Joint replacement. This surgical procedure removes and replaces an arthritic or damaged joint with an artificial joint.
Other treatments may include electrical stimulation and combination therapies to promote bone growth. It happens most commonly in the ends of a long bone. Medicines, assistive devices or surgery may be used to improve functionality or to stop further damage to the affected bone or joint. Health Home Conditions and Diseases. What causes avascular necrosis?
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