Degree Of Atrophy Research Articles

Clinicopathological Analysis of Sturge–Weber Syndrome with Focal Cortical Dysplasia FCD IIIc

Objective: To investigate the clinicopathological features of children with Sturge–Weber syndrome and to analyze the correlation between the distribution area of leptomeningeal angiomatosis, the degree of cerebral cortical calcification, and the degree of cerebral atrophy associated with epileptic seizures. Methods: 10 children were diagnosed with SWS with FCD IIIc by histopathology and immunohistochemistry. Spearman correlation analysis was used to calculate the association of SWS with FCD IIIc and seizures in children. Results: The leptomeningeal angiomatosis area was markedly positively correlated with the degree of brain atrophy in 10 children with SWS (r = 0.783, p = 0.007). The distribution of leptomeningeal hemangiomatosis, the degree of cortical calcification, and brain atrophy were not significantly correlated with epilepsy. Conclusion: SWS may be accompanied by FCD IIIc. The more extensive the cerebral lobes of leptomeningeal angiomatosis in SWS, the more pronounced the brain atrophy.

A Retrospective Study of Renal Growth Changes after Proton Beam Therapy for Pediatric Malignant Tumor.

The purpose of this study was to analyze renal late effects after proton beam therapy (PBT) for pediatric malignant tumors. A retrospective study was performed in 11 patients under 8 years of age who received PBT between 2013 and 2018. The kidney was exposed in irradiation of the primary lesion in all cases. Kidney volume and contour were measured on CT or MRI. Dose volume was calculated with a treatment-planning system. The median follow-up was 24 months (range, 11-57 months). In irradiated kidneys and control contralateral kidneys, the median volume changes were -5.63 (-20.54 to 7.20) and 5.23 (-2.01 to 16.73) mL/year; and the median % volume changes at 1 year were -8.55% (-47.52 to 15.51%) and 9.53% (-2.13 to 38.78%), respectively. The median relative volume change for irradiated kidneys at 1 year was -16.42% (-52.21 to -4.53%) relative to control kidneys. Kidneys irradiated with doses of 10, 20, 30, 40, and 50 GyE had volume reductions of 0.16%, 0.90%, 1.24%, 2.34%, and 8.2% per irradiated volume, respectively. The larger the irradiated volume, the greater the kidney volume was lost. Volume reduction was much greater in patients aged 4-7 years than in those aged 2-3 years. The results suggest that kidneys exposed to PBT in treatment of pediatric malignant tumor show continuous atrophy in follow-up. The degree of atrophy is increased with a higher radiation dose, greater irradiated volume, and older age. However, with growth and maturation, the contralateral kidney becomes progressively larger and is less affected by radiation.

Are invasive cortical stimulations effective in brain atrophy?

Electrical brain stimulation is a treatment method for brain disorder patients. The majority of patients with a severe brain disorder have brain atrophy. However, it is not clearly understood if electrical brain stimulation is effective even to brain atrophy. In this work, we developed anatomical head models with varying degrees of brain atrophy, so that we could investigate the effects of subdural/epidural cortical stimulations. The correlation between brain atrophy and cortical stimulation was quantified by calculating the effective volume that cortical stimulation influenced in this brain atrophy simulation study. The results showed that the effective volumes in both cortical stimulations decreased significantly with brain atrophy. There was also a strong correlation (0.9989) between the cerebrospinal fluid (CSF) and brain atrophy. The increase in CSF volume following brain atrophy reinforced the shunting effect between the brain and CSF and appeared to be the cause of a decrease in the stimulation effect on the brain. Overall, the epidural cortical stimulation was more sensitive (up to 57%) to the severity of the brain atrophy than the subdural cortical stimulation.

Pseudocoloboma-like maculopathy with biallelic RDH12 missense mutations

BackgroundHereditary maculopathy is a group of clinically and genetically heterogeneous disorders. With distinctive clinical features, subtypes of macular atrophy may correlate with their genetic defects.MethodsSeven patients from six families with...

Paraspinal muscles atrophy on both sides and at multiple levels after unilateral lumbar partial discectomy.

To identify the changes in cross-sectional areas (CSAs) and fatty infiltration of both sides of the paravertebral muscles and their associations with prognostic factors in patients who underwent unilateral lumbar discectomy. We retrospectively reviewed 27 patients who underwent magnetic resonance imaging before and after 1- or 2-level lumbar discectomy. The CSAs and functional cross-sectional areas of the paraspinal muscles were bilaterally measured from L1 to L2 to L5 to S1 based on T2-weighted axial images. These parameters were compared pre-and postoperatively. CSAs and functional cross-sectional areas decreased also in non-operative, non-surgical levels, not only in operated levels after discectomy. In the correlation analysis, the CSA of psoas major muscle at L1 to L2 was significantly decreased in patients with lower preoperative lordosis (r = 0.598, P = .040). The postoperative CSA of psoas major muscle at L4 to L5 was lower in those with the higher Pfirrmann grade (r = -0.590, P = .002); however, the CSA of quadratus lumborum muscle at L1 to L2 showed the opposite result (r = 0.526, P = .036). Similar results were also observed in the partial correlation adjusted for age and postoperative duration. Patients who underwent discectomy experienced overall paraspinal muscle atrophy in the lumbar region, including surgical and non-surgical sites. Such atrophic changes emphasized the need for core strengthening and lumbar rehabilitation from the early period after partial discectomy.

Characteristics of different types of Helicobacter pylori: New evidence from non-amplified white light endoscopy.

Different types of Helicobacter pylori (H. pylori) were analyzed to determine their infection characteristics using serology, pathology, and non-magnification white light endoscopy combined with the Kimura-Takemoto classification, and the regular arrangement of collecting venules (RAC) as well. A retrospective analysis of 685 inpatients who have completed the 14C-urea breath test, the H. pylori antibody typing classification, the serum gastric function tests (PGI/PGII/G-17), the endoscope detection, and the pathological examinations. The levels of PGI, PGII, and G-17 were in descending order from the type I H. pylori infection group to the type II H. pylori infection group than the control group (F = 14.31; 26.23; 9.12, P < 0.01). Using the Kimura-Takemoto classification, there were significant differences among the three groups of different degrees of atrophy ( =29.81; 482.78; 292.5, P< 0.01). Based on the characteristics of RAC, the H. pylori infection rates were in descending order from the type I H. pylori infection group to the type II H. pylori infection group than the control group ( = 200.39; 174.72; 143.51, P < 0.01). The type I H. pylori infection group had higher grades than those of the type II H. pylori infection group in the OLGA and OLGIM staging systems, while the differences are statistically significant only in the OLGA staging system ( =10.63, P < 0.05). With the aid of non-amplified white light endoscopy, we found new evidence of type I H. pylori infection accelerating the progression of gastric mucosal atrophy through the degree of atrophy and the range of infection, whereas type II H. pylori infection has a low ability of migration and atrophy progression. Individual virulence factor-based eradication therapy may be a better choice in future.

The Importance of Segment 4 Anatomy on Outcomes Following Living Donor Left Lateral Segmentectomy

BackgroundDuring left lateral section (LLS) resection for live liver donation, the vascular inflow and the bile drainage of segment 4 (S4) are compromised. We investigated the long-term changes of S4 after donation and their potential prognostic impact on living liver donors. Materials and methodsThis was a retrospective analysis of 42 consecutive left lateral (LLS, S2/3) liver resections for living donation. ResultsThere were 25 female and 17 male donors. Median age was 33 y and median body mass index was 26. Median LLS, S2/3, volume was 262 cc, and median sS4 volume was 160 cc. Complications were encountered in three donors (7%). An independent extrahepatic S4 artery (S4A) (with a proximal left heptic artery or a right hepatic artery origin) was identified in 41% of the donors. Ligation of the independent S4A was not associated with the rate of post resection liver dysfunction, complications, or the degree of S4 atrophy. Having a dominant S4 portal triad pedicle feeding the right anterior sectors, segment 5/8, of the liver was associated with increased parenchymal damage as evidenced by a higher peak of alanine aminotransferase but was not associated with postoperative complications. The median degree of atrophy of S4 at 1 y post donation as noted on imaging was 66%. The presence of a dominant S4 portal triad pedicle and the peak alanine aminotransferase early postoperatively were both predictors of the degree of S4 atrophy post donation. ConclusionsThe presence of an independent S4A or dominant S4 portal triad pedicle feeding the liver right anterior sectors, segment 5/8, should not be a contraindication for left lateral segment living donation.

Increase of ALCAM and VCAM-1 in the plasma predicts the Alzheimer's disease.

Cell adhesion molecules (CAM) are crucial in several pathological inflammation processes in Alzheimer's disease (AD). However, their potential for clinical diagnostics remains unknown. The present investigation evaluated the clinical significance of ALCAM, VCAM-1, NCAM, and ICAM-1 levels in the plasma of participants with cognitive impairment (44 patients with mild cognitive impairment, 71 patients with Alzheimer's dementia, and 18 patients with other dementia) and 28 controls with normal cognitive ability. We also detected plasma levels of multiple inflammatory factors (IFN-gamma, IL-18, IL-1beta, IL-13, IL-8, IL-7, CCL11, MCP-1, TSLP, IL-10, BDNF, IL-17, IL-5, TREM-1) using Multiplex liquid chip and plasma levels of Abeta1-42 and Abeta1-40 using liquid-phase flow cytometry (FCM). Our findings demonstrated a correlation of ALCAM and VCAM-1 with age, the severity of cognitive decline, and MTA, but no significant difference between groups for NCAM and ICAM-1. ALCAM and VCAM-1 both demonstrated a positive correlation with the degree of atrophy in the medial temporal lobe structure. Further analysis revealed no significant correlation in plasma between VCAM-1, ALCAM and Abeta1-40, Abeta1-42. Nevertheless, there was a significant correlation between VCAM-1, ALCAM and many inflammatory factors. Furthermore, the predictive value of ALCAM and VCAM-1 for AD was assessed using a multi-parameter regression model. ALCAM and VCAM-1 in combination with ApoE4, education, age, and MMSE could predict AD with high precision (AUC=0.891; AIC=146.9) without imaging diagnosis. ALCAM and VCAM-1 combination improved the predictive accuracy significantly. In a nutshell, these findings revealed ALCAM and VCAM-1 as reliable indicators of Alzheimer's disease.

Morphological examination is more effective than cell viability assays in the characterization of myotube atrophy

Skeletal muscle atrophy is a significant health problem associated particularly with aging, cancer, and metabolic diseases, leading to a decline in quality of life and responses to treatment. During skeletal muscle atrophy, the balance between protein synthesis and degradation in the tissue is disrupted in favor of protein degradation. This condition results in a reduction in muscle mass and loss of strength and function in the muscles. In order to elucidate the molecular mechanisms causing skeletal muscle atrophy, prevent the processes leading to atrophy, and test the effectiveness of emerging therapeutics, in vitro models that mimic atrophic conditions are commonly used. In these models, typically utilizing primary myoblasts obtained from tissues or myoblast cell lines, either cell viability assays or myotube morphology analyses are employed to determine the degree of atrophy occurring during differentiation. Here, the commonly used MTT cell viability assay and myotube diameter analysis were mutually evaluated to determine which one better characterizes myotube atrophy. While myotube diameter measurement can grade the extent of atrophy in myotubes, the MTT assay, although unable to directly assess the degree of myotube atrophy, demonstrated that the decrease in cell viability indicates the cause of myoblast atrophy.

Pathological analysis of lesions in the exocrine pancreas of rats induced by Zinc Maltol.

The pancreas plays an important role in the homeostasis of zinc (Zn), a nutritionally essential metal. In several previous studies, Zn ions induced inflammatory changes in the exocrine pancreas; however, little is known about Zn complexes. In this study, we microscopically, immunohistochemically, and ultrastructurally examined pancreatic lesions in Sprague-Dawley (SD) rats induced by a 4-week repeated oral dose toxicity study of Zinc Maltol (ZM), a zinc (II) complex. ZM induces acinar atrophy and increases the number of duct-like structures. Immunohistochemistry revealed a decrease in the number of trypsin-positive cells, and an increase in the number of SOX9-positive cells. Interstitial fibrosis and macrophage infiltration also correlated with the degree of acinar atrophy. Electron microscopic evaluation revealed that the acinar cells that lost granules were surrounded by fibroblasts and collagen fibers. In conclusion, we provided a detailed description of ZM-induced pancreatic lesions in SD rats.

Utility of protocol biopsy in the management of renal allograft recipients

Background: Many studies suggest that early rejection episodes and chronic changes in the allograft kidneys were often subclinical without a concomitant rise in the serum creatinine or proteinuria. Early identification of subclinical pathology by doing protocol biopsy and appropriate intervention is likely to improve long-term graft outcomes. However, it is often not done, out of concern about the procedure-related complications. Methods: All patients who underwent live donor kidney transplantation at Aster Medcity from September 2019 to August 2021 with stable graft function were included in the study. Stable graft function is defined as variation in the creatinine values of <25% from the nadir creatinine. Protocol biopsies were taken at 3 months after transplant surgery. Biopsies were done using spring-loaded biopsy guns percutaneously under ultrasound guidance, and patients were observed for 24 h in the hospital for any complication. Biopsies were analyzed by light microscopy and C4d staining and scored based on the Banff classification 2017 update. Results: Seventy patients underwent protocol kidney biopsy at a prespecified time of 3 months. Majority of our patients (74.3%) received a kidney from the first-degree blood relatives, and the rest (25.7%) of the patients received kidneys from spouses. Induction therapy was given in 57% of the patients, and the rest (43%) were transplanted without an induction agent. Of 70 specimens studied, 44 (62.9%) had normal histology and 26 (37.1%) had varying degrees of histological abnormalities. Thirteen (18.6%) had evidence of subclinical rejection, of which 12 (17.2%) showed borderline rejection and 1 (1.4%) had acute T-cell-mediated rejection (acute TCMR). Other histological findings include chronic active TCMR in 1 (1.4%), varying degrees of interstitial fibrosis and tubular atrophy in 5 (7.1%), evidence of BK virus nephropathy in 2 (2.8%), features of tacrolimus toxicity in 2 (2.8%), and acute interstitial nephritis in one patient. None of the patients developed any complication after the procedure. With appropriate treatment interventions, all patients had stable graft functions at 6-month follow-up. Conclusions: Protocol graft biopsy under real-time ultrasound guidance has a very good safety profile and can help the clinician optimize the immunosuppression with more precision, and on a long term, it might prove cost effective to the patient.

Denervation Atrophy of Skeletal Muscle is Not Influenced by Numb Levels in Mice.

Skeletal muscle undergoes rapid and extensive atrophy following nerve transection though the underlying mechanisms remain incompletely understood. We previously showed transiently elevated Notch 1 signaling in denervated skeletal muscle that was abrogated by administration of nandrolone (an anabolic steroid) combined with replacement doses of testosterone. Numb is an adaptor molecule present in myogenic precursors and skeletal muscle fibers that is vital for normal tissue repair after muscle injury and for skeletal muscle contractile function. It is unclear whether the increase in Notch signaling observed in denervated muscle contributes to denervation and whether expression of Numb in myofibers slows denervation atrophy. To address these questions, the degree of denervation atrophy, Notch signaling, and Numb expression was studied over time after denervation in C57B6J mice treated with nandrolone, nandrolone plus testosterone or vehicle. Nandrolone increased Numb expression and reduced Notch signaling. Neither nandrolone alone nor nandrolone plus testosterone changed the rate of denervation atrophy. We next compared rates of denervation atrophy between mice with conditional, tamoxifen-inducible knockout of Numb in myofibers and genetically identical mice treated with vehicle. Numb cKO had no effect on denervation atrophy in this model. Taken together, the data indicate that loss of Numb in myofibers does not alter the course of denervation atrophy and that upregulation of Numb and blunting of the denervation-atrophy induced activation of Notch do not change the course of denervation atrophy.

Update on the Epidemiology, Pathogenesis, and Biomarkers of Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most common monogenic disorder of the cerebral small blood vessels. It is caused by mutations in the NOTCH3 gene on chromosome 19, and more than 280 distinct pathogenic mutations have been reported to date. CADASIL was once considered a very rare disease with an estimated prevalence of 1.3-4.1 per 100,000 adults. However, recent large-scale genomic studies have revealed a high prevalence of pathogenic NOTCH3 variants among the general population, with the highest risk being among Asians. The disease severity and age at onset vary significantly even among individuals who carry the same NOTCH3 mutations. It is still unclear whether a significant genotype-phenotype correlation is present in CADASIL. The accumulation of granular osmiophilic material in the vasculature is a characteristic feature of CADASIL. However, the exact pathogenesis of CADASIL remains largely unclear despite various laboratory and clinical observations being made. Major hypotheses proposed so far have included aberrant NOTCH3 signaling, toxic aggregation, and abnormal matrisomes. Several characteristic features have been observed in the brain magnetic resonance images of patients with CADASIL, including subcortical lacunar lesions and white matter hyperintensities in the anterior temporal lobe or external capsule, which were useful in differentiating CADASIL from sporadic stroke in patients. The number of lacunes and the degree of brain atrophy were useful in predicting the clinical outcomes of patients with CADASIL. Several promising blood biomarkers have also recently been discovered for CADASIL, which require further research for validation.

Prognostic factors and a customized approach to anti-VEGF therapy for exudative age-related macular degeneration. Analysis of the risk of macular atrophy development

Age-related macular degeneration (AMD) is a chronic progressive multifactorial disease characterized by a degenerative process in the retinal pigment epithelium (RPE), Bruch's membrane and choriocapillaris of the fovea with secondary neuroepithelial (NE) damage. Intravitreal administration of drugs that inhibit VEGF is recognized as the only treatment for exudative form of AMD. Literature data is limited, and do not allow drawing conclusions about the influence of various factors (identified using OCT in the EDI mode) on the development of various subtypes of atrophy and their progression, so we decided to conduct our own study and research the possible timing and risks of developing various subtypes of macular atrophy in patients with exudative AMD receiving anti-VEGF therapy. As a result of the study, it was revealed that general macular atrophy (p=0.005) has a predominant effect on BCVA in the first year of the follow-up, while subtypes of atrophy anatomically less pronounced at one year of the follow-up manifest themselves only in the second year of the follow-up (p<0.05). Although color photography and autofluorescence are currently the only approved methods for assessing the degree of atrophy, the use of OCT may reveal reliable precursor endpoints that will facilitate and allow earlier and more accurate assessment of neurosensory tissue loss resulting from the atrophy. Thus, the development of macular atrophy is influenced by such parameters of disease activity as intraretinal fluid (p=0.006952), RPE detachment (p=0.001530) and the type of neovascularization (p=0.028860), as well as neurodenegerative changes in the form of drusen (p=0.011259) and cysts (p=0.042023). The new classification of atrophy according to the degree and localization of the lesion allows more differentiated conclusions about the effect of anti-VEGF drugs on the development of certain types of atrophy, which can be a decisive factor in determining the treatment tactics.

Iridocorneal Endothelial Syndrome – A Case Report

Iridocorneal endothelial (ICE) syndrome is a rare ophthalmic disorder, wherein the basic pathology is an abnormal corneal endothelium that leads to varying degrees of corneal oedema, iris atrophy, and secondary angle closure glaucoma.[1] This syndrome typically affects young women unilaterally with no family history.[2] The true aetiology of ICE syndrome is unclear. Viral cause for the disease has been proposed, based on a history of inflammation in certain cases and on the presence of inflammatory cells on histological analysis.[3] The abnormal endothelial cells may migrate posteriorly, forming a membrane that covers the adjacent structures, iris and trabecular meshwork.[4] The contraction of this membrane leads to characteristic iris changes, iridotrabecular synechiae, and corectopia with the pupil being drawn towards the area where the synechiae are most prevalent and to secondary angle-closure glaucoma.[5]

Incongruent gray matter atrophy and functional connectivity of striatal subregions in behavioral variant frontotemporal dementia.

Previous studies on the striatum demonstrated that it is involved in the regulation of cognitive function and psychiatric symptoms in patients with behavioral variant frontotemporal dementia (bvFTD). Multiple lines of evidence have shown that striatal subregions have their own functions. However, the results of the existing studies on striatal subregions are inconsistent and unclear. In this study, we found that structural imaging analysis revealed that the bvFTD patients had smaller volumes of striatal subregions than the controls. We found that the degree of atrophy varied across the striatal subregions. Additionally, the right striatal subregions were significantly more atrophic than the left in bvFTD. Functional imaging analysis revealed that bvFTD patients exhibited different changed patterns of resting-state functional connectivity (RSFC) when striatal subregions were selected as regions of interest (ROI). The RSFC extending range on the right ROIs was more significant than on the left in the same subregion. Interestingly, the RSFC of the subregions extending to the insula were consistent. In addition, the left dorsolateral putamen may be involved in executive function regulation. This suggests that incongruence in striatal subregions may be critical to the bvFTD characteristics.

Comparison of Structural Changes in Nodding Syndrome and Other Epilepsies Associated With Onchocerca volvulus.

Nodding syndrome (NS) is a unique childhood-onset epileptic disorder that occurs predominantly in several regions of sub-Saharan Africa. The disease has been associated with Onchocerca volvulus (Ov)-induced immune responses and possible cross-reactivity with host proteins. The aim of this study was to compare structural changes in the brain on MRI between NS and other forms of onchocerciasis-associated epilepsies (OAEs) and to relate structural changes to the Ov-induced immune responses and level of disability. Thirty-nine children with NS and 14 age-matched participants with other forms of OAE from an endemic region in Uganda underwent detailed clinical examination, serologic evaluation (including Ov-associated antibodies to Ov-16 and Hu-leiomodin-1) and quantitative volumetric analysis of brain MRIs (1.5 T scanner) using Neuroreader, a cloud-based software. Cerebral and cerebellar atrophy were the predominant features in both NS and OAE. On quantitative volumetric analysis, participants with NS had larger ventricular volumes compared with participants with OAE, indicative of increased global cortical atrophy (pcorr = 0.036). Among children with NS, severe disability correlated with higher degree of atrophy in the gray matter volume (pcorr = 0.009) and cerebellar volume (pcorr = 0.009). NS cases had lower anti-Ov-16 IgG signal-to-noise ratios than the OAE cases (p < 0.01), but no difference in the levels of the Hu-leiomodin-1 antibodies (p = 0.64). The levels of Ov-associated antibodies did not relate to the degree of cerebral or cerebellar atrophy in either NS or OAE cases. This is the first study to show that cerebral and cerebellar atrophy correlated with the severity of NS disability, providing an imaging marker for these endemic epileptic disorders that until now have remained poorly characterized. Both NS and OAE have cerebral and cerebellar atrophy, and the levels of Ov-associated antibodies do not seem to be related to the structural changes on MRI.

Global Cortical Atrophy Is Associated with an Unfavorable Outcome in Stroke Patients on Oral Anticoagulation

Introduction: Measures of cerebral small vessel disease (cSVD), such as white matter hyperintensities (WMH) and cerebral microbleeds (CMB), are associated with an unfavorable clinical course in stroke patients on oral anticoagulation (OAC) for atrial fibrillation (AF). Here, we investigated whether similar findings can be observed for global cortical atrophy (GCA). Methods: Registry-based prospective observational study of 320 patients treated with OAC following AF stroke. Patients underwent magnetic resonance imaging (MRI) allowing assessment of GCA. Using the simplified visual Pasquier scale, the severity of GCA was categorized as follows: 0: no atrophy, 1: mild atrophy; 2: moderate atrophy, and 3: severe atrophy. Using adjusted logistic and Cox regression analysis, we investigated the association of GCA using a composite outcome measure, comprising: (i) recurrent acute ischemic stroke (IS); (ii) intracranial hemorrhage (ICH); and (iii) death. Results: In our time to event analysis after adjusting for potential confounders (i.e., WMH, CMB, age, sex, diabetes, arterial hypertension, coronary heart disease, hyperlipidemia, and antiplatelet use), GCA was associated with an increased risk for the composite outcome in all three degrees of atrophy (grade 1: aHR 3.95, 95% CI 1.34–11.63, p = 0.013; grade 2: aHR 3.89, 95% CI 1.23–12.30, p = 0.021; grade 3: aHR 4.16, 95% CI 1.17–14.84, p = 0.028). Conclusion: GCA was associated with our composite outcome also after adjusting for other cSVD markers (i.e., CMB, WMH) and age, indicating that GCA may potentially serve as a prognostic marker for stroke patients with atrial fibrillation on oral anticoagulation.

EXPERIMENTAL JUSTIFICATION OF THE PREVENTION OF PERIODONTAL BONE TISSUE DESTRUCTION IN OVARIOECTOMIZED RATS WITH CALCIUM-CONTAINING ADDITIVES

Purpose. Study of periodontoprotective properties of preventive complexes based on calcium, quercetin, vitamins, macro- and microelements in ovariectomized rats with alimentary deficiency of protein and calcium. Materials and methods. The study was conducted on 32 female rats in which pathology of periodontal bone tissue was simulated due to hipoestrogenicity; as well as the prevention of the said pathology with biologically active complexes based on calcium citrate from the shells of Black Sea oysters and "Minerol". Hypoestrogenicity was caused by bilateral ovariectomy, the negative effect of which on bone tissue was further complicated by a diet with a low content of calcium and protein. After 5 months, the animals were removed from the experiment; the degree of atrophy of the alveolar process was determined on the drugs; the content of acid and alkaline phosphatases, elastase, catalase and MDA was determined in the homogenate of the alveolar process. Results. The combination of ovariectomy and an inferior diet caused characteristic inflammatory-dystrophic changes in the bone tissue of the jaws, which are expressed in an increase in the activity of elastase, catalase, and MDA content in the alveolar bone homogenate. Also, under the condition of pathology, an increase in the degree of atrophy of the alveolar process, an increase in the activity of acid and alkaline phosphatases was observed, which indicates a violation of mineralization processes. Prophylactic administration of a complex based on calcium citrate from the shells of Black Sea oysters and a complex based on the biologically active additive "Minerol" showed a pronounced osteoprotective effect, which consisted in the decrease of the degree of the alveolar process atrophy and the reduction of the activity of markers of bone resorption and peroxidation lipids.

MINEROL IN THE PROBABLE PREVENTION OF TOXIC IMPACT OF ION ALUMINIUM ON BONES IN RATS

Background. The use of a variety of aluminium-containing medications, occupational exposure to alumina dust and fumes, and heavily contaminated water sources have been associated with an adverse effect on the organism, in particular, on bone system. The search for a preventive means against the impact of aluminium on the state of bones is topical. Objective. To assess the probable prophylactic effect of sorbent Minerol on the skeletal system of white rats in long-term AlCl3 intoxication. Materials and methods. In the 2-month study, male rats were grouped into: intact animals; AlCl3-induced toxicity model (240 mg/kg of w.b.); and animals administered daily with Minerol 1g/kg of w.b. on the background AlCl3 intoxication. Density and content of mineral and organic components were determined in the femurs and lumbar vertebrae, with atrophy of the alveolar process being determined in the jaws. The aluminium content was determined in the femoral bones. Results. A long-term exposure to AlCl3 resulted in the 2.5-fold increase in aluminium content in femoral bones, 17.1% increase of alveolar bone atrophy, the slight decrease of the density of femoral bones and the slight increase of the density of lumbar vertebrae. The following changes in the content of the mineral-organic complex of bones were indicated: in femurs – the decrease due to both mineral and organic fractions, and in lumbar vertebrae – the increase due to significant increase in the organic fraction. Minerol reduced the aluminium content in femurs by 20.7%, caused a decrease in the density, mineral-organic component and mineral fraction of bone tissue of the femur and lumbar vertebrae, and additionally increased the degree of atrophy of the alveolar bone against the background of AlCl3 intoxication. Conclusions. In addition to the sorption effect, the dose of Minerol used in the study probably bound the nutritional components required for bone remodelling, i.e. protein, calcium, phosphorus etc. The results imply further investigations of the sorption properties of Minerol in prevention of the negative impact of AlCl3 in higher dose of the said sorbent and in combination with calcium, phosphorus and protein preparations.