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Camurati-Engelmann disease (progressive diaphyseal dysplasia) in a Moroccan family.

We report on a 46-year-old mother of Moroccan origin, suffering mainly from painful, swollen legs, and her 26-year-old son who had experienced intense pain in his legs, without fever, for approximately 3 years. They did not have dysmorphic features or abnormal gaits. Radiographic studies of the mother revealed diaphyseal sclerosis of the tibia and spondylosis of the thoracal and lumbar vertebrae. The son had sclerosis of the diaphyses of the metacarpalia of the left hand, the femur and the fibula. The other parts of the skeleton were normal. Several osteosclerotic/hyperostotic disorders, such as melorheostosis (present mostly in sporadic cases and affecting lower extremities) and van Buchem's disease (autosomal recessive and commonly affecting the mandible) were considered as a diagnosis in the proposita. However, similar symptoms in the son of the proposita suggested an autosomal dominant inheritance pattern. This brought us to the diagnosis of progressive diaphyseal dysplasia (PDD) or Camurati-Engelmann disease (CED), an autosomal dominant disorder characterized by limb pain, reduced muscle mass, weakness, a waddling gait, progressive periosteal and endosteal sclerosis of the diaphyses of the long bones and sclerosis of the skull base. Mutations in the transforming growth factor (TGF)-beta1 gene on chromosome 19q13.1 have been reported to cause this disorder. The diagnosis of PDD/CED in this family was confirmed at the molecular level by detection of a C-to-T transition at position 466, leading to an arginine-to-cysteine amino acid change (position 156) in exon 2 of the transforming growth factor-beta1 (TGFB1) gene.

Adult↗

Sclerosing bone dysplasias: genetic and radioclinical features.

Although knowledge of basic genetics in the field of sclerosing bone dysplasias is progressing, the radiologist still plays a pivotal role in the diagnosis of this relatively poorly understood group of disorders. Based on a target site approach, these anomalies are classified into three groups. Within each group, further differentiation can be made by distinctive clinical findings and by mode of inheritance: (a) dysplasias of endochondral bone formation: osteopetrosis (Albers-Schönberg disease), pycnodysostosis, enostosis, osteopoikilosis, osteopathia striata (Voorhoeve disease); (b) dysplasias of intramembranous bone formation: progressive diaphyseal dysplasia (Camurati-Engelmann disease) and variants, hyperostosis corticalis generalisata (Van Buchem disease) and variants; and (c) mixed sclerosing dysplasias: melorheostosis (Leri disease) and overlap syndromes.

Bone Diseases, Developmental↗

Juxtacortical osteoma of the ulna.

Acase of juxtacortical osteoma of the ulna in a 47-year-old woman is presented. She had a dense bony mass on the ulna. Radiological examinations (plain radiography, computed tomography, magnetic resonance imaging) strongly suggested a rare case of juxtacortical osteoma of a long tubular bone. The differential diagnosis included parosteal osteosarcoma, melorheostosis, osteochondroma, end-stage juxtacortical myositis ossificans, and fibrous dysplasia protuberans. The tumor was excised totally for thorough pathological examination, which revealed it to be composed of lamellar bone, suggesting that the origin was periosteal.

Biopsy, Needle↗

Beta ig-h3 mediates osteoblast adhesion and inhibits differentiation.

betaig-h3 is an extracellular matrix (ECM) protein induced by TGF-beta, and it has motifs interacting with the alpha3beta1, alphavbeta5, and alphavbeta3 integrins. Our previous study shows the role of betaig-h3 in osteoblast differentiation and its involvement in melorheostosis, a rare bone disease. Here we demonstrate that betaig-h3 expression is down-regulated during the early stage of differentiation of the murine preosteoblastic cell line, KS483. The recombinant betaig-h3 and its FAS1 domain significantly inhibited in vitro osteoblast differentiation as evaluated by matrix mineralization/bone nodule formation. Furthermore, inhibition of expression of osteoblast differentiation marker genes [such as type I collagen, alkaline phosphatase, and osteocalcin (OC)] was accompanied by suppression of osteoblast-specific transcription factors, Cbfa1/Runx2 and osterix. Flow cytometric analyses, cell adhesion, and inhibition assays disclosed alphavbeta3 and alphavbeta5 as the principal integrins mediating the adhesion of osteoblastic cells to betaig-h3. The disruption of interactions between betaig-h3 and osteoblasts by a function-blocking antibody specific for alphavbeta3 but not for alphavbeta5 abolished the inhibitory effect of betaig-h3 on osteoblast differentiation. We suggest that these interacting integrins may play an important role in betaig-h3-mediated inhibition of osteoblast differentiation.

Amino Acid Sequence↗

MAN1, an integral protein of the inner nuclear membrane, binds Smad2 and Smad3 and antagonizes transforming growth factor-beta signaling.

MAN1 (also known as LEMD3) is an integral protein of the inner nuclear membrane. Recently, mutations in MAN1 have been shown to result in osteopoikilosis, Buschke-Ollendorff syndrome and melorheostosis. We show that the nucleoplasmic, C-terminal domain of human MAN1 binds to Smad2 and Smad3 and antagonizes signaling by transforming growth factor-beta (TGF-beta). In a yeast two-hybrid screen using the C-terminal domain of MAN1 as bait, eight positive clones were obtained that encoded Smad3. In direct two-hybrid assays, this portion of MAN1 bound to Smad2 and Smad3. In glutathione-S-transferase precipitation assays, the C-terminal domain of MAN1 bound to Smad2 and Smad3 under stringent conditions. Antibodies against MAN1 were able to co-immunoprecipiate Smad2 from cells, demonstrating that they reside in the same complex in vivo. TGF-beta treatment stimulated transcription from a reporter gene in control cells, but reporter gene stimulation was significantly inhibited in cells overexpressing MAN1 or its C-terminal domain but not its N-terminal domain. TGF-beta-induced cell proliferation arrest was also inhibited in stable cell lines overexpressing MAN1. These results show that the nuclear envelope regulates a signal transduction pathway and have implications for how mutations in nuclear envelope proteins cause different human diseases.

Cell Line↗

From the archives of the AFIP. Extraskeletal osseous and cartilaginous tumors of the extremities.

Extraskeletal osseous and cartilaginous tumors and tumorlike conditions of the extremities can often be differentiated radiologically; for those that cannot, knowledge of the spectrum of lesions will allow a suitably ordered differential diagnosis. Of the osseous lesions--myositis ossificans, fibro-osseous pseudotumor, fibrodysplasia ossificans progressiva, soft-tissue osteoma, and extraskeletal osteosarcoma--all but myositis ossificans are relatively rare. Myositis ossificans has a distinct mineralization pattern that can be observed radiologically as a peripheral rim of lamellar bone. Fibro-osseous pseudotumor typically occurs in the digits of the hand and lacks the well-defined zoning pattern of myositis ossificans. The cartilaginous entities include the true tumors, soft-tissue chondroma and extraskeletal chondrosarcoma, and the tumorlike process, synovial osteochondromatosis. The tumors are relatively rare; synovial osteochondromatosis commonly affects middle-aged men, especially in the knee, and is associated with osteoarthritis. The differential diagnosis for these extraskeletal osseous and cartilaginous lesions includes soft-tissue sarcoma, benign mesenchymoma, malignant mesenchymoma (rare), calcified tophi in gout, melorheostosis (rare), pilomatricoma (rare), and tumoral calcinosis (rare).

Adult↗

Cortical lesions of the tibia: characteristic appearances at conventional radiography.

Lesions that involve the cortex of the tibia are fairly common in radiology practice. However, the number of diseases that involve the tibial cortex is great, and it can be difficult to arrive at a limited differential diagnosis from radiographic findings. Categorization of lesions of the tibia into those that cause cortical destruction and those that cause cortical proliferation can help narrow the broad differential diagnosis. Lesions that cause cortical destruction include nonossifying fibroma, fibrous dysplasia, osteofibrous dysplasia, aneurysmal bone cyst, giant cell tumor, eosinophilic granuloma, Ewing sarcoma, neurofibromatosis, adamantinoma, osteoblastoma, chondromyxoid fibroma, hemangioendothelioma, renal cell metastatic disease, hemangioma, and hemangiopericytoma. Lesions that cause cortical proliferation include osteochondroma, stress fracture, osteoid osteoma, periosteal osteogenic sarcoma, diaphyseal dysplasia, venous stasis, cellulitis, chronic osteomyelitis, osteopathia striatum, and melorheostosis. Conventional radiography along with clinical and pathologic data can aid in diagnosis of the wide variety of disease processes that involve the tibial cortex.

Adult↗

Diseases diagnosed in wild turkeys (Meleagris gallopavo) of the southeastern United States.

Diagnostic findings are presented on 139 sick or dead wild turkeys examined during the period 1972 through 1984. Turkeys originated from eight southeastern states (Alabama, Arkansas, Florida, Georgia, South Carolina, Tennessee, Virginia, West Virginia) and included 31 turkeys categorized as capture-related mortalities and 108 turkeys categorized as natural mortalities. Frequent diagnoses (greater than or equal to 10% of case accessions) in the natural mortality group were trauma, avian pox, and histomoniasis. Less frequent diagnoses (less than or equal to 4% of case accessions) included malnutrition/environmental stress syndrome, coligranuloma-like condition, crop impaction, bumblefoot, organophosphate toxicosis, infectious sinusitis, a lympho-proliferative disease, salmonellosis, aspergillosis, toxoplasmosis, crop trichomoniasis, and melorheostosis.

Animals↗

[Osteopoikilosis: report of 3 cases and review of the literature].

Osteopoikilosis, osteopathia condensans disseminata, is a rare hereditary autosomal dominant sclerosing bone dysplasia, more common in males. The diagnosis is usually made incidentally from radiographs which show multiple, small, well-defined, variably shaped and widely distributed (over the skeleton) sclerotic areas. The involvement is symmetrical, and the predilected locations are the phalanges of the hand, carpal bones, metacarpals, foot phalanges, metatarsals, tarsal bones, ilium, femur, radio and sacrum. It must be distinguished from melorheostosis, osteopathia striata and fundamentally from osteoblastic bone metastases, on the basis of the clinical, radiological (roentgenographs, computed tomography and magnetic resonance) and radionuclide scanning characteristics. Histologically, there are focal condensations of compact lamellar bone within the spongiosa. We report three cases of osteopoikilosis and review the literature. Two cases didn't have affectation in phalanges of the hand, which had not been previously reported, to our knowledge.

Adult↗

[Usefulness of online bibliographic research in biomedical research, with an application to the epidemiologic study of genetic osteopathy].

The bibliographic research online is an useful means of recovering information in all the subjects, particularly in the field of biomedicine. In fact, this instrument allows researchers to get information in a rapid, complete and up-to-date way. The aim of the present review is to describe the usefulness of the bibliographical research online in the field of the genetic osteopathies. These are rare disorders: so, their own rarity makes the bibliographical research online necessary to carry out a large and effective comparison of experiences. The obtained results are amply reported in the manuscript. For instance, we verified that chondrodysplasias are the diseases most represented in the literature, while melorheostosis the disorder less mentioned. Moreover, we evidenced that some hereditary disorders of connective tissue, such as Marfan's syndrome, osteogenesis imperfecta and Ehlers-Danlos syndrome, are strongly influenced by race, sex and age.

Bibliometrics↗

Linear melorheostotic scleroderma with hypertrichosis.

On the basis of clinical features and histological findings, cutaneous manifestations of linear melorheostotic scleroderma are apparently derived from a localized proliferative disorder and are not secondary to bone changes. If the hypertrichosis has the same origin as the osteocutaneous changes, melorheostosis may represent a congenital disorder with both ectodermic and mesodermic components.

Adult↗

[Pseudoscleroderma and sclerodermiform states].

Pseudo-scleroderma should not be confused with true scleroderma, the prognosis of which is unpredictable and often serious. Progressive acrosclerosis must be differentiated from Raynaud's disease, congenital or hereditary disorders of unknown aetiology: Werner's syndrome, acrogeria and progeria; Rothmund-Thomson's syndrome, Steinert's disease, phenylketonuria, disorders of glycogen metabolism; metabolic disorders: mutilating acropathies, scleromyxoedema, porphyria cutanea tarda; occupational and iatrogenic disorders: acroosteolysis, toxic epidermic syndrome (Spain), scleroderma-like change induced by bleomycin, chronic graft-versus-host disease; and leprosy. Acute diffuse scleroderma should not be confused with Buschke's scleroedema, sclerema neonatorum, systemic amyloidosis and scleroderma-like changes in hypothyroidism. Linear pseudo-scleroderma is suggested by the following scleroderma-like conditions: facial hemiatrophy, acrodermatitis atrophicans, melorheostosis, pseudo-scleroderma after corticosteroid injection, and cutaneous lesions in carcinoid syndrome. Scleroderma in plaque must be differentiated from hypodermitis sclerotisans, panatrophy and localized lipoatrophies, hypodermitis after vitamin K injection, basal cell carcinoma, necrobiosis lipoidica, vitiligo, chronic radiodermatitis, cutaneous lymphatic invasion. Scleroderma-like changes after drug injection (vitamin B12, progestin), anetoderma barely resemble morphea guttata.

Adipose Tissue↗

[Striated osteopathy].

Striated osteopathy, a roentgenological entity characterized by longitudinal striations, can occur concomitantly with a number of disorders which should be routinely looked for. There are three types of striated osteopathy. The pure form without severe bone disorders is the form originally reported by Voorhoeve. In the second form, there is a concomitant fibrous dysplasia, such as Jaffe-Lichtenstein-Uehlinger disease, Ollier enchondromatosis, sponastrism dysplasia, or osteopetrosis. This group also includes bone dysplasias with sclerosis such as melorheostosis, osteopecilia, and sclerosis of the base of the skull which is sometimes seen in patients with striated osteopathy. In the third form, striated osteopathy occurs concomitantly with a skin disease such as patchy dermal hypoplasia or hyperpigmented skin lesions.

Child↗