Pathologic Basis of Diseaseby Stanley L. Robbins is really the fourth edition of hisPathology. Appropriate updating and addition enhance the otherwise identical format, sequence, writing, and illustrations. So many medical students have benefited from this source that it may be the best known general book in the field. I recommend it even more now. Like his former texts, this will be enjoyed for its readability. He clearly lays out a great deal of information. When he includes minutiae, the reasons are clear and one feels that all the material is pertinent. Robbins keeps the whole field in perspective—that is, he does not dwell so long or so heavily on pathologic anatomy or pathogenesis as to tempt the reader to overlook clinical presentation or prognosis. A great strength of the subject of pathology is that it bonds strongly with many other medical sciences and specialties and thus occupies the

Pathologic Basis of Disease

British authors are the natural heirs to Charles Dickens and Graham Greene.) Nevertheless there are advantages to British readers in a British book especially, for instance, in the chapter on social paediatrics and occasionally as regards therapeutics. The new Forfar and Arneil is, like its predecessors, a good book. There are many new authors and much of it has been completely rewritten. Each chapter has a long list of references, many of them to further reading in books and important 'landmark' papers rather than to very recent original work, and that seems appropriate for a textbook of this nature. It is up to date, including references to topics such as oesophageal pH monitoring in gastrooesophageal reflux, the value of steroids in bacterial meningitis, a full account of the peroxisomal disorders, the significance of dystrophin in muscular dystrophy, the importance of vitamin A in reducing mortality in third world countries, and the use of sumatriptan in migraine and of vigabatrin and lamotrigine in epilepsy. Surprisingly, neither in this nor in Nelson's textbook could I find any reference to Angelman's syndrome. Some topics chosen at random such as Prader-Willi syndrome or haemolytic uraemic syndrome were discussed more fully in the British textbook. There is a surprising omission, however, and that is the chapter on disorders ofear, nose, and throat. Adenoids, glue ear or secretory otitis media, tonsillitis, and tonsillectomy have all been dropped from the index and deafness is dealt with in the chapter on neurology. If you look up 'tonsils' you will be referred to any entry which reads: 'Tonsils: size, presence of infection, exudate, pitting, peritonsillar swelling?'. The index entry 'ear, nose and throat problems' refers to a brief account of such problems in children with cleft palate. It is one of those crazy facts of modern life that the American book costs £60, the British £125. Who will read this new edition? I shall, and I suppose many other consultant paediatricians will also use it as a standard reference book. Undergraduate students will need a more compact text for their basic reading but should use it to look up specific topics, and doctors studying for the MRCP in paediatrics should make a systematic assault on it to provide them with a personal database to be supplemented by journals and monographs. As a textbook of British paediatrics it has no competition and it remains an excellent work of reference which must be available in all paediatric departments in Britain, but the absence of the chapter on ear, nose, and throat disorders must surely be an error and there is clearly a marketing problem for British publishers faced with American competition. If we want British textbooks, and I would not like to think that the time will be forced upon us when we shall have no choice, then it looks as if we must be prepared to pay for the privilege. DOUG ADDY Consultant paediatrician

https://adc.bmj.com/content/archdischild/68/3/435.2.full.pdf

Syndromes of the Head and Neck

Tumor-induced osteomalacia (TIO) is a rare and fascinating paraneoplastic syndrome in which patients present with bone pain, fractures, and muscle weakness. The cause is high blood levels of the recently identified phosphate and vitamin D-regulating hormone, fibroblast growth factor 23 (FGF23). In TIO, FGF23 is secreted by mesenchymal tumors that are usually benign, but are typically very small and difficult to locate. FGF23 acts primarily at the renal tubule and impairs phosphate reabsorption and 1α-hydroxylation of 25-hydroxyvitamin D, leading to hypophosphatemia and low levels of 1,25-dihydroxy vitamin D. A step-wise approach utilizing functional imaging (F-18 fluorodeoxyglucose positron emission tomography and octreotide scintigraphy) followed by anatomical imaging (computed tomography and/or magnetic resonance imaging), and, if needed, selective venous sampling with measurement of FGF23 is usually successful in locating the tumors. For tumors that cannot be located, medical treatment with phosphate supplements and active vitamin D (calcitriol or alphacalcidiol) is usually successful; however, the medical regimen can be cumbersome and associated with complications. This review summarizes the current understanding of the pathophysiology of the disease and provides guidance in evaluating and treating these patients. Novel imaging modalities and medical treatments, which hold promise for the future, are also reviewed.

/pdf/tumor-induced-osteomalacia-3jzki3qja5.pdf

Tumor-induced osteomalacia

The present review will give an update on temporomandibular joint (TMJ) imaging using CBCT. It will focus on diagnostic accuracy and the value of CBCT compared with other imaging modalities for the evaluation of TMJs in different categories of patients; osteoarthritis (OA), juvenile OA, rheumatoid arthritis and related joint diseases, juvenile idiopathic arthritis and other intra-articular conditions. Finally, sections on other aspects of CBCT research related to the TMJ, clinical decision-making and concluding remarks are added. CBCT has emerged as a cost- and dose-effective imaging modality for the diagnostic assessment of a variety of TMJ conditions. The imaging modality has been found to be superior to conventional radiographical examinations as well as MRI in assessment of the TMJ. However, it should be emphasized that the diagnostic information obtained is limited to the morphology of the osseous joint components, cortical bone integrity and subcortical bone destruction/production. For evaluation of soft-tissue abnormalities, MRI is mandatory. There is an obvious need for research on the impact of CBCT examinations on patient outcome.

/pdf/temporomandibular-joint-diagnostics-using-cbct-2c5va10l3l.pdf

Temporomandibular joint diagnostics using CBCT

Fibroblast growth factors (FGF) and their receptors serve many functions in both the developing and adult organism. Humans contain 18 FGF ligands and four FGF receptors (FGFR). FGF ligands are polypeptide growth factors that regulate several developmental processes including cellular proliferation, differentiation, and migration, morphogenesis, and patterning. FGF-FGFR signaling is also critical to the developing axial and craniofacial skeleton. In particular, the signaling cascade has been implicated in intramembranous ossification of cranial bones as well as cranial suture homeostasis. In the adult, FGFs and FGFRs are crucial for tissue repair. FGF signaling generally follows one of three transduction pathways: RAS/MAP kinase, PI3/AKT, or PLCγ. Each pathway likely regulates specific cellular behaviors. Inappropriate expression of FGF and improper activation of FGFRs are associated with various pathologic conditions, unregulated cell growth, and tumorigenesis. Additionally, aberrant signaling has been implicated in many skeletal abnormalities including achondroplasia and craniosynostosis. The biology and mechanisms of the FGF family have been the subject of significant research over the past 30 years. Recently, work has focused on the therapeutic targeting and potential of FGF ligands and their associated receptors. The majority of FGF-related therapy is aimed at age-related disorders. Increased understanding of FGF signaling and biology may reveal additional therapeutic roles, both in utero and postnatally. This review discusses the role of FGF signaling in general physiologic and pathologic embryogenesis and further explores it within the context of skeletal development.

Fibroblast growth factor (FGF) signaling in development and skeletal diseases.

There have been no quantitative standards for volumetric and surface measurements of the mandibular condyle in Caucasian population. However, the recently developed cone-beam computed tomography (CBCT) system allows measurement of these parameters with high accuracy. CBCT was used to measure the condylar volume, surface and the volume to surface ratio, called the Morphometric Index (MI), of 300 temporo-mandibular joints (TMJ) in 150 Caucasian young adult subjects, with varied malocclusions, without pain or dysfunction of TMJs. The condylar volume was 691.26 ± 54.52 mm3 in males and 669.65 ± 58.80 mm3 in, and was significantly higher (p< 0.001) in the males. The same was observed for the condylar surface, although without statistical significance (406.02 ± 55.22 mm2 in males and 394.77 ± 60.73 mm2 in females). Furthermore, the condylar volume (693.61 ± 62.82 mm3 ) in the right TMJ was significantly higher than in the left (666.99 ± 48.67 mm3, p < 0.001) as was the condylar surface (411.24 ± 57.99 mm2 in the right TMJ and 389.41 ± 56.63 mm2 in the left TMJ; t = 3.29; p < 0.01). The MI is 1.72 ± 0.17 for the whole sample, with no significant difference between males and females or the right and left sides. These data from temporomandibular joints of patients without pain or clinical dysfunction might serve as examples of normal TMJ's in the general population not seeking orthodontic care.

/pdf/condylar-volume-and-surface-in-caucasian-young-adult-36jpxt1896.pdf

Condylar volume and surface in Caucasian young adult subjects

This Provisional PDF corresponds to the article as it appeared upon acceptance. Fully formatted PDF and full text (HTML) versions will be made available soon. Condylar volume and surface in Caucasian young adult subjects

Oncogenic osteomalacia is an uncommon syndrome characterized by bone pain, proximal muscle weakness, hypophosphatemia, hyperphosphaturia, and a low plasma concentration of 1,25-dihydroxy-vitamin D. The disease affects both sexes at around 40 years of age, although it can sometimes affect children and adolescents. Generally, the syndrome is associated with a tumor, usually benign, of mesenchymal origin and is resolved after removal of the tumor; this syndrome can sometimes be associated with malignant tumors. These tumors seem to be histologically heterogeneous and are generally localized in soft tissues and bone. In this article, a case of oncogenic osteomalacia associated with a hypophosphaturic mesenchymal tumor of the ethmoid is reported in a 24-year-old man. After surgical and radical removal of the tumor, the patient noted a decrease in the clinical symptoms and signs.

Hypophosphaturic mesenchymal tumor of the ethmoid associated with oncogenic osteomalacia.

Craniosynostosis, both isolated and syndromic, are challenging malformations for the craniofacial team. They present the team with an articulated cascade of choices, which need to be addressed early in life and in the growing age to intercept, remove, or correct the direct and indirect consequences of the malformation. Timing of treatment is thus critical and it stands on the experience of a multi-specialty trained craniofacial team. In this paper the authors discuss the timing of treatment of the major craniosynostosis, isolated and syndromic, reviewing the options for treatment and their experience in this complex field.

Surgical timing of craniosynostosis: what to do and when.

There are no quantitative standards for the volumetric measurements of the orbital cavity after Le Fort III advancement. Computed tomography (CT) scan images have given the opportunity to compare with accuracy the real anatomic changes and potentially the functional improvements that resulted after a surgical treatment.Three-dimensional CT scan images processed by DICOM files in Dolphin 3D Software were used to assess orbital volume and surface in 12 subjects affected by craniofacial syndromic malformations treated with Le Fort III advancement. The preoperative (T0) and postoperative (T1: 6 months after surgery) three-dimensional craniofacial CT scans of the subjects were collected and retrospectively analyzed. Image segmentation of the anatomic orbital cavity and the three-dimensional graphic rendering were done by using the Dolphin Imaging Plus 11.0 software.The orbital volume was increased after surgery, with statistical significance, from 22,267 to 22,706.3 mm(3) in the right eye and from 26,511 mm(3) to 26,256.4 mm(3) in the left eye. The surface of both bony orbits had an expansion, which is statistically significant. In conclusion, this study showed that the orbital advancement in white subjects after Le Fort III advancement was significant and produced a significant augmentation of the orbital volume and surface area with correction of the ocular bulb proptosis.

Orbital Volume and Surface After Le Fort III Advancement in Syndromic Craniosynostosis

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