Relevant bibliographies by topics / Osteitis fibrosa

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Academic literature on the topic 'Osteitis fibrosa'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Osteitis fibrosa"

1

Gavrić, Nikola. "Osteitis fibrosa cystica generalisata." Scripta Medica 37, no. 2 (2006): 101–3. http://dx.doi.org/10.5937/scrimed0602101g.

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Agstam, Sourabh. "Osteitis fibrosa cystica." Indian Journal of Nephrology 30, no. 6 (2020): 433. http://dx.doi.org/10.4103/ijn.ijn_292_19.

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Cherian, E. T., and K. B. Guttenberg. "Osteitis fibrosa cystica." QJM: An International Journal of Medicine 111, no. 7 (February 5, 2018): 487. http://dx.doi.org/10.1093/qjmed/hcy019.

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Ramon, Andre, and Pierre-Emmanuel Berthod. "Osteitis Fibrosa Cystica." New England Journal of Medicine 382, no. 11 (March 12, 2020): e15. http://dx.doi.org/10.1056/nejmicm1907828.

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Arbault, Anaïs, Paul Ornetti, Davy Laroche, and Pierre Pottecher. "Osteitis fibrosa cystica." Joint Bone Spine 84, no. 2 (March 2017): 229. http://dx.doi.org/10.1016/j.jbspin.2016.02.027.

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Maanaoui, Mehdi, Aghiles Hamroun, Céline Lebas, Rémi Lenain, and Arnaud Lionet. "Osteitis fibrosa cystica von Recklinghausen." Journal of Nephrology 34, no. 3 (February 8, 2021): 925–26. http://dx.doi.org/10.1007/s40620-020-00961-4.

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7

Shin, Sug Kyun, Do Hun Kim, Heung Su Kim, Kyu Tae Shin, Kyung Ae Ma, Sung Jung Kim, Youn Sik Kwak, Seung Kyu Ha, and Donald J. Sherrard. "Renal Osteodystrophy in Pre-Dialysis Patients: Ethnic Difference?" Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 19, no. 2_suppl (February 1999): 402–7. http://dx.doi.org/10.1177/089686089901902s65.

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The purpose of the present study is to investigate whether an ethnic difference exists in the incidence of renal osteodystrophy between Asian and Western countries in end-stage renal disease (ESRD) patients. We evaluated bone histology in 58 pre-dialysis patients (28 male, 30 female; mean age: 47.7 years). All patients had bone biopsies with quantitative histomorphometry and sero-logical parameters such as intact PTH, osteocalcin, total alkaline phosphatase, and basal and deferoxamine-stimulated serum aluminum levels. We observed that 91.4% of all evaluated patients showed renal osteodystrophy before the start of dialytic therapy. Mild osteitis fibrosa were observed in 21 patients (36.2%), severe osteitis fibrosa in 5 patients (8.6%), mixed lesions in 7 patients (12.1 %), osteomalacia in 6 patients (10.3%), aplastic bone disease in 14 patients (24.1%), and normal bone in 5 patients (8.6%). Among the bone histomorphometric parameters, fibrosis area rate (%) showed the best correlation with intact PTH, and osteocalcin and osteoid area rate (%) with total alkaline phosphatase. Aluminum-related bone disease was not observed. Among patients with aplastic bone disease, only 14.3% showed aluminum deposition of any significance (5% < stainable bone surface aluminum < 25%). In the diabetic patients, aplastic bone disease was most common, but no case was related to aluminum intoxication. In conclusion, the distribution of renal osteodystrophy in our study was different from that of Western countries in pre-dialysis patients. Our patients tended to have more mild-form osteitis fibrosa and normal findings, and less severe-form osteitis fibrosa and aplastic bone disease. Aluminum-related bone disease was not observed.
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Seo, D., and Y. Rhee. "Osteitis fibrosa cystica in primary hyperparathyroidism." QJM 108, no. 12 (August 9, 2015): 991. http://dx.doi.org/10.1093/qjmed/hcv144.

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Rodríguez-Gutiérrez, René, and José Miguel Hinojosa-Amaya. "Brown Tumors: Severe Osteitis Fibrosa Cystica." Mayo Clinic Proceedings 90, no. 5 (May 2015): 699–700. http://dx.doi.org/10.1016/j.mayocp.2014.08.025.

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Phitayakorn, Roy, and Christopher R. McHenry. "Jaw Tumor: An Uncommon Presenting Manifestation of Primary Hyperparathyroidism." World Journal of Endocrine Surgery 2, no. 1 (2010): 45–50. http://dx.doi.org/10.5005/jp-journals-10002-1021.

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ABSTRACT Introduction To report two unusual cases of primary hyperparathyroidism (HPT) that initially manifested with a “ jaw tumor” and to discuss the clinical implications of a giant cell granuloma vs an ossifying fibroma of the jaw. Material and methods The history, physical examination, laboratory values and the imaging and pathologic findings are described in two patients who presented with a “jaw tumor” and were subsequently diagnosed with primary HPT. The diagnosis and management of osteitis fibrosa cystica and HPT-jaw tumor syndrome are reviewed. Results Patient #1 was a 70-year-old male who presented with hypercalcemia, severe jaw pain, and an enlarging mass in his mandible. Biopsy of the mass revealed a giant cell tumor and he was subsequently diagnosed with primary HPT. A sestamibi scan demonstrated a single focus of abnormal radiotracer accumulation, corresponding to a 13,470 mg parathyroid adenoma, which was resected. Postoperatively, the serum calcium normalized and the giant cell granuloma regressed spontaneously. Patient #2 was a 36-year-old male with four incidentally discovered tumors of the mandible and maxilla, who was diagnosed with normocalcemic HPT and vitamin D deficiency. Biopsy of one of the tumors revealed an ossifying fibroma. Bilateral neck exploration revealed a 2480 mg right inferior parathyroid adenoma, which was resected. Postoperative genetic testing revealed an HRPT2 gene mutation. He subsequently underwent resection of an enlarging ossifying fibroma of the mandible with secondary reconstruction. Conclusions A “jaw tumor” in a patient with primary HPT may be a manifestation of osteitis fibrosa cystica or HPT-jaw tumor syndrome underscoring the importance of biopsy and genetic testing for management and follow-up.
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Dissertations / Theses on the topic "Osteitis fibrosa"

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Garau, Agostino. "Cementoblastoma mandibular: caso clínico." Master's thesis, 2021. http://hdl.handle.net/10284/10702.

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O cementoblastoma é uma lesão benigna rara que representa menos de 1% a 6% de todos os tumores odontogénicos (Milani et al. 2012; Borges et al. 2019). Caracteriza-se pela proliferação de tecido tipo cimento e tende a estar associado a um dente permanente erupçionado, sendo o mais prevalente o primeiro molar. Neste trabalho é apresentado um caso clinico, pouco relatado na literatura face às suas dimensões, de um cementoblastoma que afetou o corpo mandibular esquerdo, estendendo-se do canino ao primeiro pré-molar, de uma mulher de 15 anos de idade. Foi realizada uma cirurgia sob anestesia geral, tendo sido excitada a exérese total da lesão e tendo a mesma sido enviada para análise histológica. A particularidade do seguinte caso foi a estrutura remanescente óssea extremamente fragilizada após a remoção da lesão, que apresentava um tamanho de 28×24 mm. Esta fragilidade levou a necessidade de utilização de placas de osteossíntese e bloqueio intermaxilar procurando evitar fratura iatrogénica da mandibula, conjuntamente a loca cirúrgica foi regenerada com um enxerto de crista ilíaca conjuntamente com osso autologo e sintético. A paciente foi monitorizada durante 9 meses após a cirurgia e não mostrou quaisquer sinais de recidiva.
Cementoblastoma is a rare benign lesion that represents less than 1% to 6% of all odontogenic tumours (Milani et al. 2012; Borges et al. 2019). It is characterised by proliferation of cementum-like tissue and in all cases tends to be associated with an erupting permanent tooth, most often the first molar. This paper presents a clinical case, little reported in the literature due to its dimensions, of a cementoblastoma that affected the left mandibular body, extending from the canine to the first premolar, of a 15-year-old woman. Surgery was performed under general anaesthesia, with total excision of the lesion being excited and sent for histological analysis. The particularity of the following case was the extremely fragile bone remnant structure after the removal of the lesion, which had a size of 28×24 mm. This fragility led to the need to use osteosynthesis plates and intermaxillary blockage, seeking to avoid iatrogenic fracture of the mandible, together with the surgical site being regenerated with an iliac crest graft together with autologous and synthetic bone. The patient was monitored for 9 months after surgery and showed no signs of recurrence.
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Books on the topic "Osteitis fibrosa"

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German Society for Osteology. Conference. Generalized bone diseases: Osteoporosis, osteomalacia, ostitis fibrosa. Berlin: Springer-Verlag, 1987.

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Kuhlencordt, F., P. Dietsch, and E. Keck. Generalized Bone Diseases: Osteoporosis, Osteomalacia, Ostitis Fibrosa. Springer, 1988.

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Sprague, Stuart M., and James M. Pullman. Spectrum of bone pathologies in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0122.

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Histologic bone abnormalities begin very early in the course of chronic kidney disease. The KDIGO guidelines recommend that bone disease in patients with chronic kidney disease should be diagnosed on the basis of bone biopsy examination, with bone histomorphometry. They have also proposed a new classification system (TMV), using three key features of bone histology—turnover, mineralization, and volume—to describe bone disease in these patients. However, bone biopsy is still rarely performed today, as it involves an invasive procedure and highly specialized laboratory techniques. High-turnover bone disease (osteitis fibrosa cystica) is mainly related to secondary hyperparathyroidism and is characterized by increased rates of both bone formation and resorption, with extensive osteoclast and osteoblast activity, and a progressive increase in peritrabecular marrow space fibrosis. On the other hand, low-turnover (adynamic) bone disease involves a decline in osteoblast and osteoclast activities, reduced new bone formation and mineralization, and endosteal fibrosis. The pathophysiological mechanisms of adynamic bone include vitamin D deficiency, hyperphosphataemia, metabolic acidosis, inflammation, low oestrogen and testosterone levels, bone resistance to parathyroid hormone, and high serum fibroblast growth factor 23. Mixed uraemic osteodystrophy describes a combination of osteitis fibrosa and mineralization defect. In the past few decades, an increase in the prevalence of mixed uraemic osteodystrophy and adynamic bone disease has been observed.
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Bardin, Thomas, and Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.

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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.
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Book chapters on the topic "Osteitis fibrosa"

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Sakr, Mahmoud F. "Osteitis Fibrosa Cystica." In Parathyroid Gland Disorders, 149–71. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07418-9_8.

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Theisler, Charles. "Osteitis Fibrosa Cystica." In Adjuvant Medical Care, 245–46. New York: CRC Press, 2022. http://dx.doi.org/10.1201/b22898-253.

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Agarwal, Amit, Ranil Fernando, Rajeev Parameswaran, Anand Mishra, and Roma Pradhan. "PHPT Presenting as Osteitis Fibrosa Cystica." In Case Studies in Thyroid and Parathyroid Tumors, 3–7. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-0938-4_1.

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"Osteitis fibrosa cystica." In Dermatology Therapy, 432. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_1990.

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"Osteitis fibrosa disseminata." In Dermatology Therapy, 432. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/3-540-29668-9_1991.

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6

"osteitis fibrosa, n." In Oxford English Dictionary. 3rd ed. Oxford University Press, 2023. http://dx.doi.org/10.1093/oed/2659192977.

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González, Esther A., and Kevin J. Martin. "Cytokines and growth factors in renal bone disease." In The Spectrum of Renal Osteodystrophy, 159–84. Oxford University PressNew York, NY, 2001. http://dx.doi.org/10.1093/oso/9780192632302.003.0007.

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Abstract Renal bone disease or renal osteodystrophy is a common complication of chronic renal failure and represents a spectrum of skeletal abnormalities ranging from high turnover states, such as osteitis fibrosa which is seen with secondary hyperparathyroidism, to states of low bone turnover which include osteomalacia and the increasingly common adynamic bone disease. While each of these abnormalities may be predominant in a specific patient, combinations of these patterns are commonly present. Histologically, osteitis fibrosa is characterized by increased bone turnover with increased osteoblast and osteoclast number and activity leading to increased bone formation and increased bone resorption. An additional feature of osteitis fibrosa, as the name implies, is the presence of endosteal and marrow fibrosis. In contrast, in adynamic bone disease, there is decreased bone turnover, with decreased number and activity of osteoblasts and osteoclasts.
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Fournier, Albert, Philippe Morinière, Roxana Oprisiu, Adriana Albu Tataru, Said Said, Michel Brazier, Annick Marié, Martine Esther Cohen Solal, and Abderahman Ghazali. "Adynamic bone disease in uremia." In The Spectrum of Renal Osteodystrophy, 227–68. Oxford University PressNew York, NY, 2001. http://dx.doi.org/10.1093/oso/9780192632302.003.0009.

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Abstract For the sake of clarity it must first be stressed that the definition of adynamic (or aplastic) bone disease (ABD) and that of osteoporosis are based on criteria of different nature. Adynamic bone disease is a histopathological pattern which has been individualized among the various types of renal osteodystrophy by Sherrard et al. in hypercalcemic uremic patients because it did not coincide with formerly individualized entities, namely osteitis fibrosa, osteomalacia, and mixed lesions. In spite of hypercalcemia, osteoclastic bone resorption was not increased as in osteitis fibrosa, and in contrast to osteomalacia osteoid volume and thickness were not increased. Actually only osteoid surface may be increased in ABD. As in osteomalacia, however, osteoblastic surfaces were scarce or absent, explaining the low bone formation rate (BFR).
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Felsenfeld, Arnold J., and Armando Torres. "Osteitis fibrosa, osteomalacia, and mixed bone lesions." In The Spectrum of Renal Osteodystrophy, 185–226. Oxford University PressNew York, NY, 2001. http://dx.doi.org/10.1093/oso/9780192632302.003.0008.

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Abstract To fully comprehend renal osteodystrophy today, it is important to appreciate its long and interesting history. Because the primary focus of this chapter is not a historical review, it is necessary to provide a selective, personal perspective of historical studies. It should also be emphasized that until the late 1960s, descriptions of renal osteodystrophy were in patients who had never received dialysis and thus were not exposed to potential modifying factors such as aluminum or increased calcium delivery during dialysis. Aluminum exposure produced a form of osteomalacia not previously observed in the azotemic patient and the improved calcium balance produced by dialysis may have modified the bone disease either directly by increasing serum calcium or indirectly by the suppression of parathyroid hormone (PTH).
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Ritz, Eberhard, Michael Schömig, and Giulio Odoni. "Medical therapy in dialysis patients." In The Spectrum of Renal Osteodystrophy, 473–90. Oxford University PressNew York, NY, 2001. http://dx.doi.org/10.1093/oso/9780192632302.003.0019.

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Abstract There is consensus that development of secondary hyperparathyroidism should be prevented in the pre-dialytic stage of renal failure (see Chapter 18 in this issue). The sad reality is that the majority of patients reach end-stage renal failure without seeing a nephrologist and without appropriate management of disturbed calcium phosphate metabolism. As a result, hyperparathyroidism and osteitis fibrosa continue to be a problem. This is all the more important since Mizumoto documented that the strongest predictor of uncontrollable advanced hyperparathyroidism on dialysis was the PTH concentration at the time of admission to renal replacement therapy. Uncontrolled evidence from Nordal also suggests that bony lesions in uremic patients can only be reliably prevented if vitamin D treatment had started early. In the past, the major problem in dialyzed patients was uncontrolled hyperparathyroidism and osteitis fibrosa. More recently, the frequency of advanced hyperparathyroidism, although still high, has diminished. The situation has become more complex, however, because a variety of other skeletal problems have gained clinical importance. Although the tragic episode of bone disease from aluminum intoxication is a chapter of the past, at least in Western Europe, other skeletal problems such as f32m-amyloidosis, bone loss (osteopenia), particularly in post-menopausal women, and the very controversial entity of ‘low bone turnover’, so-called adynamic bone disease, have gained prominence. The clinical significance of high bone turnover is uncertain. It predisposes to hypercalcemia, but whether the bone fracture rate is increased is controversial and not very plausible in view of the absence of bone fractures in non-renal patients with hypoparathyroidism. Ideally, maintenance hemodialysis should be only a stage of transit until patients are transplanted. According to dialysis registries6 a failed transplant has become a major reason for renal replacement therapy. Consequently, late consequences of steroid therapy have also become more frequent.
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