Cause Of Calcification Research Articles

Percutaneous endoscopic lumbar endoscopic discectomy in L5-S1 calcified disc herniation

Introduction: Calcified lumbar intervertebral disc herniation is a special type of herniated disc, the cause of which is still poorly understood. Chronic inflammation is proposed as a possible cause of calcification. Calcification can occur in the herniated nucleus pulposus when the course of the lumbar herniated disc has been> 6 months. A hard disk increases the stenosis of the nerve root canal and therefore causes compressive symptoms giving dysesthesia in the lower extremities. Most patients will need open surgery as well as subsequent decompression and instrumentation. Percutaneous Endoscopic Lumbar Discectomy, using minimally invasive techniques, is a safe alternative treatment for calcified herniated discs. Case Presentation: We present the case of a 34-year-old male patient, Police on active duty, with severe low back pain according to the Pain Scale (VAS) of 8 and Oswestry Index of Disability also disabled (56%), in addition to radiculopathy of the long lower left limb evolution, without apparent cause and exacerbated 6 months ago. Magnetic resonance imaging shows a left foraminal paracentral paracentral protrusion hernia with morphological changes like calcification and with L5-S1 caudal migration, in addition to a severe narrowing of the canal. Conclusions: Percutaneous Endoscopic Lumbar Discectomy is a safe procedure that allows, with minimal invasion techniques, to decompress the medullary canal despite having significant narrowing. It also does not destroy healthy tissue unnecessarily or sacrifice stability. Lastly, a lower incidence of complications is reported.

Diagnostic Findings and Surgical Management of Three Dogs Affected by Osseous Metaplasia Secondary to a Salivary Mucocele.

Saliva is an irritant of the subcutaneous tissue, thus causing the development of a non-epithelial reactive pseudocapsule. Metaplastic ossification of the pseudocapsule is a condition rarely described in the veterinary literature. The main causes of calcification are trauma, tumours, various chronic inflammatory conditions and fibrodysplasia ossificans progressiva. The aim of the present case series was to describe three dogs affected by a calcified salivary mucocele. The medical records of dogs affected by a cervical sialocele were retrospectively evaluated, and three cases met the inclusion criteria. All the dogs in this study were referred to the Veterinary Teaching Hospital (VTH) of the Department of Veterinary Sciences of the University of Turin (Turin, Italy) for a large solid mass in the intermandibular region. The diagnosis of a mucocele was confirmed clinically by centesis and by radiography or CT. Complete excision of both the pseudocyst and the ipsilateral mandibular/monostomatic sublingual salivary gland was performed in all cases. The histological report showed large areas of bone metaplasia within the pseudocapsule and chronic sialadenitis. Based on this limited case series, complete excision of the pseudocyst and a concurrent sialoadenectomy provided an effective treatment for this rare salivary mucocele disorder.

Патогенез и клинические проявления ювенильной и сенильной форм болезни Фара (научный обзор)

В научном обзоре на основе анализа литературных источников представлен сложный патогенез развития неатеросклеротического симметричного обызвествления базальных ядер (болезнь Фара). Представлена оригинальная таблица основных причин кальцификации вещества головного мозга. Приведены основные направления в лечении описываемой патологии.

Дифференциальный клинико-морфологический подход в изучении кальцинатов плаценты

Objective: to detect possible causes of calcification of the placenta, identify patterns between excessive deposition of fibrinoid, calcium salts and various disorders in the mother-placenta-fetus system. Materials and methods. 6,089 afterbirths and placental tissue sections were examined, of which 193 specimens complying with the purpose of the study were further studied and divided into three groups (group of biological norm; afterbirths in which there is fibrinoid deposition without accompanying calcification; afterbirths with pronounced deposits of calcium salts). Each section of placental tissue was studied macro- and microscopically according to the method of A.P. Milovanov and A.I. Brusilovsky to reveal structural and functional changes. Statistical processing of the results was performed using methods of descriptive statistics, nonparametric methods: compilation of contingency tables, calculation of Pearson's χ2 test with Yates correction. Results. It was found that all the afterbirths studied had similar macroscopic characteristics. Microscopic examination revealed that calcification contributes to a more pronounced separation of the lobules of the maternal part of the placenta. Various inflammatory, alterative processes, as well as hemodynamic disorders in the placental tissue contribute to the deposition of calcium salts. Conclusion. The involutive processes observed in normal aging of the placenta become most pronounced in various pathological processes in the mother-fetus-placenta system. The study revealed a statistically significant relationship between the number of labor and the appearance of calcifications in the placental tissue. Large focal deposits of calcium salts were more often observed in women who gave birth not for the first time.

108 Infertility from retained fetal bone after termination: Case report and literature review

Primary Objective: To review the literature addressing symptoms of retained fetal content after termination. Secondary objective: To discuss a case of hysteroscopic management in a patient with retained fetal bone content after remote termination procedure. Case report and literature review in an Urban based healthcare system of a patient who underwent hysteroscopic removal of retained fetal bone after remote history of surgical termination. This report describes the case of a 37-year-old woman presenting for infertility who had a termination of pregnancy at 20 weeks 17 years prior. Upon ultrasound echogenic structures were seen in the cervix and further confirmed with MRI. Hysteroscopy revealed mature fetal bone which was then removed. Literature Review: In the literature, similar cases have an original presentation of secondary infertility. Studies of the underlying pathophysiology have shown that these patients have prostaglandin levels similar to those with intrauterine devices (IUD) (6). Thus, retained fetal bone in the uterus may cause an environment in the uterus similar to an IUD resulting in secondary infertility. Other instances of retained bone have been attributed to osseous metaplasia secondary to chronic inflammation of the uterus (7). This in addition to other causes of calcification must remain in the differential until ruled out. Retained products are not uncommon in patients with termination at an advanced gestational age. The presented case portrays an unusual finding in an infertility patient remote from her termination episode. Review of the images in this case may help providers consider retained bone as an alternative to causes of infertility in patients with a history of termination.

Diagnosis, Management, and Percutaneous Sampling of Nipple-Areolar Calcifications: How Radiologists Can Help Patients Avoid the Operating Room.

Both benign and malignant causes of calcifications in the nipple-areolar complex exist. BI-RADS terminology applies to the description and classification of nipple-areolar calcifications in the same way it does to calcifications elsewhere in the breast. Minimally invasive sampling can be performed safely and accurately with ultrasound-guided techniques, with a few technical modifications. This article provides insight regarding the management algorithm and image-guided interventional techniques for sampling nipple-areolar calcifications as an essential competency for breast imaging practices.

Bilateral Calcification of Basal Ganglia in a Patient with Duplication of Both 11q13.1q22.1 and 4q35.2 with New Phenotypic Features

We report on a female patient who presented with severe intellectual disability and autistic behavior, dysmorphic features, orodental anomalies, and bilateral calcification of basal ganglia. Using a high-density oligonucleotide microarray, we have identified a de novo duplication of 11q13.1q22.1 involving the dosage sensitive genes FGF3 and FGF4, genes related to autosomal dominant disorders KMT5B, GAL, SPTBN2, and LRP5, susceptibility loci SCZD2, SLEH1, and SHANK2, mitochondrial genes NDUFV1, NDUFS8, and TMEM126B, and many loss of function genes, including PHOX2A, CLPB, MED17, B3GNT1, LIPT2, and CLPB. However, the duplication did not involve Ribonuclease H2, subunit C (RNASEH2C) which is considered to be located in the critical region for Aicardi-Goutières syndrome. In combination with the duplication at 11q13.1, a 1.849-Mb heterozygous duplication at 4q35.2 was also identified. Although this duplicated region does not contain causative genes related to brain calcification, the duplication at 4q35 was reported previously in a patient with basal ganglia calcification, coats' like retinopathy, and glomerulosclerosis. Our patient's presentation and genomic findings indicate that duplication of 4q35.2 could be a novel genetic cause of calcification of basal ganglia. Our report also underscores the clinical significance of rearrangements in 11q13.1q22.1 in the pathogenesis of basal ganglia calcification.

Identifying Coronary Artery Calcification on Non-gated Computed Tomography Scans.

Coronary artery calcification (CAC) provides an objective measure of coronary artery disease and can readily be identified on non-gated computed tomography (CT) scans with a high correlation with gated cardiac CT scans. This standardized protocol takes a step-wise approach to not only optimizing an image for the identification of calcification but also to distinguishing CAC from other common causes of calcification in the cardiac silhouette. Recognition of CAC on non-gated CT scans helps to identify a very powerful prognostic factor that can influence therapeutic interventions or downstream diagnostic testing without requiring a gated cardiac scan. These non-gated CT scans are often acquired as part of the routine care of the patient, and this data is readily available without another dose ofionizing radiation. This protocol allows for the precise and accurate extraction of this data for the purposes of retrospective data analysis in clinical research studies, but also in the clinical evaluation and management of patients.

Analysis of the Differences in the Microbial Community and Structure of Calcified ONP Granular Sludge and Bagasse Granular Sludge

Anaerobic biological technology has been widely used in the treatment of high-concentration organic wastewater such as old newspaper (ONP) pulping wastewater and bagasse spray washing wastewater before pulping. However, due to the high calcium content and complex chemical properties of the ONP pulping wastewater, granular sludge calcification occurs during the anaerobic treatment, which has negative effects. In contrast, calcification does not occur in the bagasse spray washing wastewater. Therefore, a comparative analysis of the biological flora and structure of the granular sludge for these two types of wastewater can provide theoretical and data support for revealing the cause of calcification of granular sludge. The results indicate a considerable difference between the anaerobic granular sludge for the treatment of bagasse spraying wastewater (B-GS) and the treatment of ONP pulping wastewater (P-GS). The microorganisms in the B-GS were mainly Bactericides (25.4%), Proteobacteria (20.2%), Hyd24－12 (14.4%), Chloroflexi (10.6%), and Firmicutes (8.9%). The microorganisms in the P-GS were mainly Bacteroidetes (20.4%), Chloroflexi (19.5%), Proteobacteria (19.3%), Firmicutes (6.2%), Spirochaetae (4.8%), Actinobacteria (4.4%), and Lentisphaerae (4.3%). Methanomassiliicoccus were detected only in the P-GS. The methanogens had a higher relative abundance in the P-GS (50%), and only a small fraction (10%) of methanogens was detected in the B-GS.

Calcifications of the parotid space. A review

Parotid lithiasis is the main cause of calcifications in the parotid space. However, there are many other less known causes. The aim of our study was to point out the non-lithiasic causes of calcifications in the parotid space. We conducted an exhaustive review of the literature by mean of PubMed, using the keywords "parotid" and "calcification" and limiting our analysis to the original articles in humans published in English and in French. Articles reporting about microscopic calcifications and who were not dealing with parotid calcifications were excluded. Twenty articles met the inclusion criterions. Tumoral and non-tumoral local causes and systemic causes of parotid calcification were found. The way they revealed was variable. The main tumoral local causes were pleomorphic adenomas, salivary duct carcinomas and adenocarcinomas. The main non-tumoral local causes included vascular malformations and calcified parotid lymph nodes. The main systemic causes were chronic kidney diseases, HIV infection, chronic alcoholism, elevated levels of alkaline phosphatase and auto-immune diseases. Eighteen different etiologies of parotid space calcifications could be identified. First line exploration of these lesions relies mainly on conventional radiography and ultrasound examination that are easily available. CT scan remains the reference examination.

Invivo efficacy for novel combined anticalcification treatment of glutaraldehyde-fixed cardiac xenograft using humanized mice.

The animal immune response against Galα1,3-Galβ1-4GlcNAc-R(α-Gal) epitopes gives an important cause for the failure of glutaraldehyde(GA)-fixed cardiac xenografts. This study aimed to assess the invivo effect of our novel combined anticalcification treatment, which includes immunologic modification, using α1,3-galactosyltransferase knock-out mice to mimic human immunologic environment. Bovine pericardia were cross-linked with GA and treated with decellularization, immunologic modification with α-galactosidase, space-filler with polyethylene glycol, organic solvent, and detoxification. The bovine pericardia were subcutaneously implanted into humanized and wild type mice, and titers of anti α-Gal IgM and IgG were evaluated at various time intervals. Invivo calcification and immunohistochemistry staining was assessed for the explanted xenografts several months after implantation. In humanized mice, titers for anti α-Gal IgM and IgG increased as the period of implantation increased, and reduced with our anticalcification treatments. The humanized mice had more invivo calcification in GA-fixed xenografts treated with our anticalcification protocol compared with wild type mice. In humanized mice, invivo calcification reduced with our combined anticalcification treatment, and the immunohistochemistry of the harvested xenografts proved the compatible findings with the results of invivo immunogenicity and calcification. Humanized mice are effective model for the assessment of invivo calcification, and our combined anticalcification treatments reduced invivo calcification as well as invivo immunogenicity in humanized mice group, suggesting that the animal immune reaction is the cause for calcification. Our novel combined anticalcification strategies of decellularization, immunologic modification, space-filler, organic solvent, and detoxification have possible promise to prolong the lifespan of cardiac xenograft.

BuMPy road of delayed graft function

BuMPy road of delayed graft function

Radiological Features of Soft Tissue Calcification: A Pictorial Essay

Calcification of soft tissue may represent a nonspecific local response or be a manifestation of underlying disease. The diagnosis and principle of treatment varies depending on the characteristics of the calcified lesions. Soft tissue calcification is classified by mechanism into 3 types: metastatic calcifications, calcinosis, and dystrophic calcifications. However, classification according to the site and shape of calcification may be more helpful for a clinical diagnosis. The purpose of this pictorial essay is to classify soft tissue calcifications according to their location: vessel, periarticular, joint capsule, tendon, bursa, cartilage, ligament, and in tumors, as well as to document the characteristic radiological findings and causes of calcifications.

Hepatic Artery Calcification in a Liver Transplant Recipient

The abdominal aorta and the renal, mesenteric, and splenic arteries are frequently affected with arterial wall calcification upon increasing age; the hepatic artery is far less often found to be calcified. We report the case of a liver transplant recipient who presented with a calcified hepatic artery in the liver graft 13 years after transplantation for primary sclerosing cholangitis. Although the etiology of hepatic artery calcification was unknown, underlying causes for calcification may include chronic hemodialysis for renal insufficiency and subsequent secondary hyperparathyroidism, as well as a calcified aneurysms. However, it remained unclear whether hepatic artery calcification had to be considered an epiphenomenon or an original pathology of the liver. It thus seems unlikely that hepatic artery calcification as a single finding is to be considered a serious pathologic entity, even for a liver graft.

A Case of Tumoral Calcinosis at the Auricle

Tumoral calcinosis is characterized by the deposition of calcium phosphate in periarticular soft tissues and mainly occurs around large joints of the hips, shoulders, and elbows. However, it oc-curs very rarely at the auricle. The etiology of tumoral calcinosis is unknown with a greater prev-alence among blacks. Tumoral calcinosis must be differentiated from other more common causes of calcification. The most effective treatment for a tumoral calcinosis is complete surgical exci-sion. Recently, we experienced a case of tumoral calcinosis at the right auricle in a 10 year-old male patient. So we report this case with the literature review.

Calcified Integra membrane: one possible cause of skin graft failure in the second stage of Integra use

The use of Integra as an artificial dermal regeneration template is well established. Following initial use of Integra to resurface the wound bed, the second stage involves removal of the silicone layer and application of a split skin autograft. Previous histological studies have shown that neo-vascularisation of the Integra occurs between 2 and 4 weeks, and therefore, skin grafting over the Integra is recommended at any time after this period. We present a case of an infant with 38% total percentage of body surface area in whom we performed early burn excision and immediate application of Integra. In this case, the second stage of skin grafting was delayed, resulting in the formation of a crusty white membrane over the Integra. Histological analysis with a Von Kossa stain revealed evidence of calcification within the superficial layers of the Integra. Each leg was initially treated differently. In one leg, mechanical scrubbing of this layer was performed. The subsequent results of grafting in this leg were unsatisfactory, and repeat grafting was necessary. In the other leg, tangential excision using a Watson knife was performed before grafting. This produced much better results in terms of skin graft ‘take’. The causes of calcification in biomaterials are discussed, and recommendations are made on the basis of the clinical findings in this particular case.

Idiopathic vulvar calcinosis: The counterpart of idiopathic scrotal calcinosis

Calcinosis cutis is characterized by the deposition of hydroxyapatite crystals of calcium phosphate in the skin. It is commonly encountered as a consequence of connective tissue disease or metabolic abnormalities but sometimes could be idiopathic. We report a case of idiopathic calcinosis cutis of the vulva in a healthy woman. A 35-year-old woman presented with multiple asymptomatic yellowish nodules on the external genitalia of one year duration. A few of the nodules broke down spontaneously discharging a chalky white material. She was otherwise healthy and had no systemic complaints. There was neither a history of trauma nor any inflammatory process in the vulvar skin prior to the development of lesions. The hematologic and biochemistry panel such as liver and renal function, serum calcium, phosphorous, electrolytes, uric acid and parathyroid hormone levels were normal. An excision biopsy of the nodule showed features suggestive of calcinosis cutis (Fig. 1). Fig. 1 10× photomicrograph showing the amorphous calcific deposits in the dermis Cutaneous calcification may be divided into four major categories: dystrophic, metastatic, iatrogenic and idiopathic.1 Though dystrophic calcinosis is fairly common, idiopathic calcification is rare, and usually no underlying cutaneous cause can be identified. It commonly presents as painless, firm papules and nodules that appear in childhood and adolescence and gradually increase in number and size. Lesions may be solitary or pedunculated and are initially skin-colored, but as they grow larger they become yellowish and lobulated breaking down spontaneously or when compressed to produce a chalky white material. Microscopic examination typically shows large granular deposits of deeply basophilic material which stains black with Von Kossa stain for calcium.2 The pathogenesis of idiopathic vulvar calcinosis is highly disputed. The principle debate concerning the cause is whether calcium is deposited at the site of inflamed epidermal cysts or whether the calcific nodules are truly idiopathic. Although several authors have suggested that vulvar calcinosis results from dystrophic calcification of the inflammed epidermal cysts, several others have refuted the above facts and found it to be truly idiopathic.3 Idiopathic calcinosis cutis of the vulva is rare with only seven cases reported worldwide. Besides, it has also been reported over the neck after rhytidectomy,4 the sctotal wall5, shaft of the penis6 and the areola of the breast.7 Cornelius et al, have postulated that tiny apatite crystals seen only on electron microscopy in cases of idiopathic calcinosis cutis might act as a source of injury leading to secondary deposition of acid mucopolysaccharides, which become a matrix for crystal formation and calcification. What initiates the deposition of these crystals is not yet known.8 In our case no predisposing cause for calcification could be identified and since the patient was asymptomatic and not keen on surgical removal the lesions were not excised.

Tissue Heart Valve Mineralization: Review of Calcification Mechanisms and Strategies for Prevention:

Attempts to replace diseased human valves with prostheses began more than 30 yrs ago. Heart valve prostheses can be broadly classified into mechanical prostheses (made out of non-biological materials) and bioprostheses made out of biological tissue. Biological valves are made from animal tissue bovine pericardium and porcine valves. The use of these tissues became commercially available after the introduction of the glutaraldehyde (GA) fixation technique. GA reacts with tissue proteins to form inter- and intramolecular crosslinks, resulting in improved durability. The advantage of bioprostheses compared with mechanical valves is the freedom from thromboembolism; and therefore, the avoidance of long-term anticoagulation therapy. These prostheses are preferable in elderly people and in patients who do not tolerate anticoagulants. However, tissular calcification and primary tissue failure (caused by the mechanical stress) are the main unresolved problems. The causes of calcification are numerous and, to date, a satisfactory solution to this question has not been found, although chemical treatments with metal cations, diphosphonates and treatments eliminating phospholipids have proved to mitigate calcification. In addition, alterna-tive approaches to GA chemical treatment fixation are being proposed to provide the tissue with greater resistance to this process. Studies are under way using polyepoxy compounds, derivates of amino oleic acid (AOA), agents such as diphenylphosphorylazide, carbodiimide, amino acids etc. Further improvements in fixation techniques, as well as in bioprosthesis design (stentless valves) are being made to improve the durability and functional characteristics of bioprosthetic heart valves. The development of a biomaterial capable of withstanding calcification and mechanical stress, while being as durable as mechanical prostheses, would convert the bioprostheses into the replacement of choice by eliminating the need for anticoagulation therapy.

Tissue heart valve mineralization: Review of calcification mechanisms and strategies for prevention.

Attempts to replace diseased human valves with prostheses began more than 30 yrs ago. Heart valve prostheses can be broadly classified into mechanical prostheses (made out of non-biological materials) and bioprostheses made out of biological tissue. Biological valves are made from animal tissue bovine pericardium and porcine valves. The use of these tissues became commercially available after the introduction of the glutaraldehyde (GA) fixation technique. GA reacts with tissue proteins to form inter- and intramolecular crosslinks, resulting in improved durability. The advantage of bioprostheses compared with mechanical valves is the freedom from thromboembolism; and therefore, the avoidance of long-term anticoagulation therapy. These prostheses are preferable in elderly people and in patients who do not tolerate anticoagulants. However, tissular calcification and primary tissue failure (caused by the mechanical stress) are the main unresolved problems. The causes of calcification are numerous and, to date, a satisfactory solution to this question has not been found, although chemical treatments with metal cations, diphosphonates and treatments eliminating phospholipids have proved to mitigate calcification. In addition, alterna-tive approaches to GA chemical treatment fixation are being proposed to provide the tissue with greater resistance to this process. Studies are under way using polyepoxy compounds, derivates of amino oleic acid (AOA), agents such as diphenylphosphorylazide, carbodiimide, amino acids etc. Further improvements in fixation techniques, as well as in bioprosthesis design (stentless valves) are being made to improve the durability and functional characteristics of bioprosthetic heart valves. The development of a biomaterial capable of withstanding calcification and mechanical stress, while being as durable as mechanical prostheses, would convert the bioprostheses into the replacement of choice by eliminating the need for anticoagulation therapy.

Peritoneal calcification: causes and distinguishing features on CT.

We undertook this study to determine the causes of peritoneal calcification seen on CT and to investigate which CT features distinguish benign from malignant peritoneal calcification. Seventeen patients with peritoneal calcification were identified through retrospective review of reports from 74765 abdominopelvic CT examinations performed during a 7-year period. We determined the cause of peritoneal calcification by examining medical and histopathologic records. Calcification morphology was classified as nodular or sheetlike on the basis of the consensus interpretation by two independent radiologists. The radiologists also recorded the presence or absence of associated soft-tissue components or lymph node calcification. The association between the CT findings and the cause of calcification was assessed using chi-square analysis. Peritoneal calcification was due to peritoneal dialysis (n = 4), prior peritonitis (n = 3), cryptogenic origin (n = 1), or peritoneal spread of ovarian carcinoma (n = 9). Sheet-like calcification was more common in patients with benign calcification (seven of eight patients) than in those with malignant calcification (two of nine patients, p < 0.05). Nodal calcification was seen only in patients with malignant calcification (five of nine patients vs none of eight, p < 0.05). Common causes of peritoneal calcification are dialysis, prior peritonitis, or ovarian cancer; sheetlike calcification indicates a benign cause, whereas associated lymph node calcification strongly suggests malignancy.