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Sinonasal tumours
Published in Neeraj Sethi, R. James A. England, Neil de Zoysa, Head, Neck and Thyroid Surgery, 2020
Yujay Ramakrishnan, Shahzada Ahmed
Ossifying fibroma is also a condition where normal bone is replaced by fibrous tissue. It is usually diagnosed in patients in their 30s and 40s. It preferentially affects the mandible (75%) or maxilla (10%–20%). The exact pathophysiology is not clearly understood [19].
McCune−Albright Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Fibro-osseous lesions are a diverse group of processes that may be developmental (hamartomatous), reactive, dysplastic, or neoplastic [8,9]. Based on Waldron's classification system, fibro-osseous lesions of jaws consist of: (i) fibrous dysplasia, (ii) cemento-osseous dysplasia (fibro-osseous or cemental lesions presumably arising in the periodontal ligament), and (iii) ossifying fibroma (fibro-osseous neoplasms of uncertain or detectable relationship to those arising in the periodontal ligament) (Table 44.2) [10]. Ossifying fibroma differs from fibrous dysplasia by having a well-circumscribed and sharply defined margin [11].
The Frontal Sinus
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
The nomenclature surrounding ossifying fibroma (OF) is diverse and confusing. Broadly, OF can be classified into 3 categories:116Ossifying fibromaCemento-ossifying fibroma (COF)Aggressive psammomatoid ossifying fibroma (APOF) or juvenile-aggressive OF. These benign tumours can have differing biologic behaviour. Histologically, lesions consist of 2 main components: fibrous stroma and bone elements. APOF lesions consist of irregular bony spicules within a cellular fibrous stroma. Classically, this resembles cementum or calcified ‘psammomatoid bodies’. COF lesions have similar histologic features with cementum-like material present throughout the lesion.
Frontal osteoplastic flap without frontal sinus obliteration for orbital roof decompression
Published in Orbit, 2021
Matthew Kim, Marc Otten, Michael Kazim, David A. Gudis
FD usually develops early in life, presenting by the third decade with typical symptoms of orbitocranial FD including headache and craniofacial asymmetry or deformity.3 Slow and progressive growth can lead to more devastating sequelae, especially in the limited confines of the orbit, including visual impairment and even loss of vision. Imaging reveals a lesion with “ground glass” appearance, and the hallmark of FD is the lack of a distinct radiographic border between the lesion and normal bone.2–4 Biopsy generally serves to confirm the diagnosis, although the wide histopathologic overlap among the 3 BFOL pathologies necessitates multimodal diagnostic workup, reconciling pathologic and radiographic findings.2,5,6 Particularly for ossifying fibroma (OF), the relatively poor correlation between radiographic and pathologic findings warrants early or proactive tissue sampling, along with the proclivity of these lesions to exhibit destructive and expansile growth and to recur.7
Osteocalcin, Azan and Toluidine blue staining in fibrous dysplasia and ossifying fibroma of the jaws
Published in Alexandria Journal of Medicine, 2018
Samuel Ebele Udeabor, Akinyele Olumuyiwa Adisa, Anna Orlowska, Poju Chia, Robert A. Sader, Shahram Ghanaati
Fibrous dysplasia (FD) and ossifying fibroma (OF) are fibro-osseous lesions (FOLs). FOLs are diverse jaw disorders characterized by the replacement of normal bone with benign fibrous connective tissue matrix and a secondary attempt at new bone formation.1–3 Although there are some differences in the biologic behavior, clinical presentation and radiography of these two lesions, there are several overlaps that may make final diagnosis difficult.4 The histology of the two lesions, again, is so similar, that it is virtually impossible to make a diagnosis of either one of them based on histology alone. The basis for final diagnosis and clear objectivity is therefore called into question. So, with overlapping clinical presentation and indistinct histology, reliable diagnosis can only be reached by further investigations.
Tumor-induced osteomalacia caused by a massive phosphaturic mesenchymal tumor of the acetabulum: A case report
Published in Modern Rheumatology, 2018
Kimitaka Nakamura, Masanobu Ohishi, Tomoya Matsunobu, Yasuharu Nakashima, Akio Sakamoto, Akira Maekawa, Yoshinao Oda, Yukihide Iwamoto
Tumors that are responsible for TIO include PMT, GCT, fibrous dysplasia, osteosarcoma, and so on [8–10]. Based on histopathology, Weidner et al. subdivided PMTs into four categories: (i) phosphaturic mesenchymal tumor mixed connective tissue (PMTMCT) variant, (ii) osteoblastoma-like variant, (iii) non-ossifying fibroma-like variant, and (iv) ossifying fibroma-like variant [8]. The majority of FGF-23-producing tumors responsible for TIO are considered to be of the PMTMCT variant [11]. Jiang et al. reported that 46% of the tumors responsible for TIO were PMTMCT [10].