Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “OSSIFICATION, PATHOLOGIC”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources

Sonography of the coccyx in newborns and infants.

The ultrasonic appearance of the coccyx was studied in 61 newborn infants and young children without known congenital abnormalities. The coccyx was easily seen in all children as a hypoechoic structure with a variable number of vertebral body ossification centers. Knowledge of the normal appearance of the coccyx can prevent confusion with pathologic conditions such as abscesses or tumors and can be helpful in the detection of congenital coccygeal abnormalities.

Cartilage↗

Thoracic spondylosis: experience of 4 cases.

Thoracic spondylosis is relatively uncommon compared to cervical or lumbar spondylosis. It may cause spinal canal stenosis and result in radiculopathy, neurogenic claudication, and most commonly, myelopathy. We present our experience in the management of 4 cases with symptomatic thoracic spondylosis. The lower thoracic spine was involved in all 4 cases. The pathological changes are almost the same as in cervical or lumbar spondylosis except that ossification of ligamenta flava is more common in thoracic spondylosis. The ossified ligamenta flava may adhere tightly to the dura mater, and therefore increase the difficulty of operation. The results of decompressive laminectomy for thoracic spondylosis were acceptable.

Adult↗

The value of enhanced magnetic resonance imaging in the evaluation of endocochlear disease.

BACKGROUND: Gadolinium-enhanced magnetic resonance imaging (GdMRI) is routinely used in the evaluation and management of suspected retrocochlear pathology such as vestibular schwannoma. However, its value in the evaluation and diagnosis of cochlear pathology associated with sensorineural hearing loss (SNHL) has been less clear. STUDY DESIGN: Retrospective review of case histories and imaging studies of patients with SNHL and cochlear enhancement on GdMRI diagnosed between 1998 and 2000. RESULTS: Five patients with SNHL who required gadolinium administration to establish the diagnosis of endocochlear disease were identified. Diagnosed lesions included an intralabyrinthine schwannoma, intracochlear hemorrhage, radiation-induced ischemic change, autoimmune labyrinthitis, and meningogenic labyrinthitis. In these illustrative cases, the GdMRI demonstrated intrinsic high signal or contrast enhancement within the cochlea and labyrinth in the absence of a retrocochlear mass. In one patient with meningogenic labyrinthitis, cochlear enhancement on MRI led to prompt cochlear implantation before the potential development of cochlear ossification. CONCLUSION: Our experience suggests that GdMRI plays a crucial role in the diagnosis of cochlear pathology associated with sensorineural hearing loss and may directly impact patient management.

Adult↗

From genotype to phenotype: the differential expression of FGF, FGFR, and TGFbeta genes characterizes human cranioskeletal development and reflects clinical presentation in FGFR syndromes.

Mutations in the fibroblast growth factor receptor (FGFR) genes 1, 2, and 3 are causal in a number of craniofacial dysostosis syndromes featuring craniosynostosis with basicranial and midfacial deformity. Great clinical variability is displayed in the pathologic phenotypes encountered. To investigate the influence of developmental genetics on clinical diversity in these syndromes, the expression of several genes implicated in their pathology was studied at sequential stages of normal human embryo-fetal cranial base and facial ossification (n = 6). At 8 weeks of gestation, FGFR1, FGFR2, and FGFR3 are equally expressed throughout the predifferentiated mesenchyme of the cranium, the endochondral skull base, and midfacial mesenchyme. Both clinically significant isoforms of FGFR2, IgIIIa/c and IgIIIa/b, are coexpressed in maxillary and basicranial ossification. By 10 to 13 weeks, FGFR1 and FGFR2 are broadly expressed in epithelia, osteogenic, and chondrogenic cell lineages. FGFR3, however, is maximally expressed in dental epithelia and proliferating chondrocytes of the skull base, but poorly expressed in the osteogenic tissues of the midface. FGF2 and FGF4, but not FGF7, and TGFbeta1 and TGFbeta3 are expressed throughout both osteogenic and chondrogenic tissues in early human craniofacial skeletogenesis. Maximal FGFR expression in the skull base proposes a pivotal role for syndromic growth dysplasia at this site. Paucity of FGFR3 expression in human midfacial development correlates with the relatively benign human mutant FGFR3 midfacial phenotypes. The regulation of FGFR expression in human craniofacial skeletogenesis against background excess ligand and selected cofactors may therefore play a profound role in the pathologic craniofacial development of children bearing FGFR mutations.

Craniofacial Dysostosis↗

Heterotopic ossification.

Heterotopic ossification, the formation of bone in soft tissue, requires inductive signaling pathways, inducible osteoprogenitor cells, and a heterotopic environment conducive to osteogenesis. Little is known about the molecular pathogenesis of this condition. Research into two rare heritable and developmental forms, fibrodysplasia ossificans progressiva and progressive osseous heteroplasia, has provided clinical, pathologic, and genetic insights. In fibrodysplasia ossificans progressiva, overexpression of bone morphogenetic protein 4 and underexpression of multiple antagonists of this protein highlight the potential role of a potent morphogenetic gradient. Research on fibrodysplasia ossificans progressiva also has led to the identification of the genetic cause of progressive osseous heteroplasia: inactivating mutations in the alpha subunit of the gene coding for the stimulatory G protein of adenylyl cyclase. Better understanding of the complex developmental and molecular pathology of these disorders may lead to more effective strategies to prevent and treat other, more common forms of heterotopic ossification.

Adolescent↗

Gene expression in human osteoblastic cells from normal and heterotopic ossification.

Heterotopic ossification (HO), a possible complication of head injury, develops in sites where it is not normally present like at the vicinity of joints. It may cause pain, decrease motion and in severe cases complete joint ankylosis requiring surgical intervention. To our knowledge, no study has been made to analyze HO at the molecular level on human biopsies, whereas its etiology remains to be determined. We defined a procedure of cell fractionation from bone resections and developed quantitative RT-PCR to compare genetic expression patterns between human normal osteoblasts and heterotopic ossification forming cells. This quantitative study demonstrated a specific and strong overexpression of osteocalcin mRNA in HO-isolated cells associated with a significant upregulation of type 1 collagen and osteonectin mRNA while histological analysis showed only small cellular variations. Our results give a first molecular characterization of heterotopic ossification and we conclude that such overexpressions in HO-isolated cells could be associated with the high activity of this pathological bone.

Adult↗

CT of postmeningitic deafness: observations and predictive value for cochlear implants in children.

PURPOSE: To demonstrate CT abnormalities encountered in children with postmeningitic deafness and to assess the value of CT in the prediction of cochlear implantation difficulties. METHODS: Thirteen children with postmeningitic deafness were evaluated with high-resolution, thin-section CT. CT findings were correlated with surgical anatomy at the time of cochlear implantation, with particular regard to the prediction of implant success. RESULTS: CT findings included normal scans (3 of 13, 23.1%), cochlear stenosis (5 of 13, 37.7%), cochlear fibroossific change (1 of 13, 7.7%), cochlear ossification (4 of 13, 30.8%), and osseous hypertrophy at the round window niche (4 of 13, 30.8%). Nine of 10 patients with abnormal findings had incomplete or difficult implantations (90%); 7 (88.8%) of these 9 received limited electrode insertions. CONCLUSION: Attention to subtle otological abnormalities on thin-section CT is helpful in the prediction of early success or failure of implantation in children with postmeningitic deafness. Those with CT abnormalities had a 90% risk of incomplete or difficult insertions with a 70% chance of limited electrode insertion.

Adolescent↗

Radionuclide bone scanning of medullary chondrosarcoma.

Technetium-99m methylene diphosphonate bone scans of 18 medullary chondrosarcomas of bone were correlated with pathologic macrosections of the resected tumors. There was increased scan uptake by all 18 tumors, and the uptake in 15 scans corresponded accurately to the anatomic extent of the tumors. Only three scans displayed increased uptake beyond the true tumor margins; thus, the "extended pattern of uptake" beyond the true tumor extent is much less common in medullary chondrosarcomas than in many other primary bone tumors. Therefore, increased uptake beyond the apparent radiographic margin of the tumor suggests possible occult tumor spread. Pathologically, there was intense reactive new bone formation and hyperemia around the periphery of all 18 tumors, and there were foci of enchondral ossification, hyperemia, or calcification within the tumor itself in nearly every tumor. Three scans displayed less uptake in the center of the tumors than around their peripheries. One of these tumors was necrotic in the center, but the other two were pathologically no different from tumors that displayed homogeneous uptake on the scan.

Bone Neoplasms↗

[Progressive fragmentation of a bipartite patella: apropos of a case].

PURPOSE OF THE STUDY: Progressive dissolution of the supero-lateral fragment of a bipartite patella is reported. MATERIAL AND METHODS: The patient, a 44 year old professor of gymnastics, was examined for long standing anterior knee pain. For many years, his daily activities included forceful knee flexion exercises. Serial radiographs, between 1986 and 1990, revealed a progressive fragmentation of the accessory ossification center and accompanying calcific deposits in the lateral patellar retinaculum. RESULTS: Surgical excision of the calcific mass and accessory ossification center relieved the painful symptomatology completely, allowing the patient full normal function at one year's follow-up. DISCUSSION: The pathological findings were compatible with a dystrophic calcinosis associated with detritic synovitis. A pathogenic mechanism is hypothesized for this unusual and progressive course of a common condition: Repetitive trauma, in this case forceful knee flexion exercises, shear microscopic bony fragments of the poorly vascularized accessory ossification center. These microscopic fragments act as deposits of an apatite crystal which go on to induce the secondary soft tissue calcifications seen in our patient.

Adult↗

Bilateral dystrophic ossification of the thyroid cartilage appearing as symmetrical laryngeal masses.

Primary cartilaginous lesions of the larynx are relatively uncommon. We present a case of bilaterally pseudocystic lesion of the thyroid cartilage that demonstrated progressive calcification. Pathologic analysis showed features suggesting a dystrophic lesion with no evidence of malignancy. We hypothesize that repetitive microtrauma related to muscular overuse probably led to inflammatory changes at tendinous insertions on the laryngeal cartilage and resulted in dystrophic ossification of the laryngeal cartilage.

Adult↗

Connective tissue growth factor: what's in a name?

Connective tissue growth factor (CTGF) is a member of the recently described CCN gene family which contains CTGF itself, cyr61, nov, elm1, Cop1, and WISP-3. CTGF is transcriptionally activated by several factors although its stimulation by transforming growth factor beta (TGF-beta) has attracted considerable attention. CTGF acts to promote fibroblast proliferation, migration, adhesion, and extracellular matrix formation, and its overproduction is proposed to play a major role in pathways that lead to fibrosis, especially those that are TGF-beta-dependent. This includes fibrosis of major organs, fibroproliferative diseases, and scarring. CTGF also appears to play a role in the extracellular matrix remodeling that occurs in normal physiological processes such as embryogenesis, implantation, and wound healing. However, recent advances have shown that CTGF is involved in diverse autocrine or paracrine actions in several other cell types such as vascular endothelial cells, epithelial cells, neuronal cells, vascular smooth muscle cells, and cells of supportive skeletal tissues. Moreover, in some circumstances CTGF has negative effects on cell growth in that it can be antimitotic and apoptotic. In light of these discoveries, CTGF has been implicated in a diverse variety of processes that include neovascularization, transdifferentiation, neuronal scarring, atherosclerosis, cartilage differentiation, and endochondral ossification. CTGF has thus emerged as a potential important effector molecule in both physiological and pathological processes and has provided a new target for therapeutic intervention in fibrotic diseases.

Amino Acid Sequence↗

The clinicopathological features of three babies with osteogenesis imperfecta resulting from the substitution of glycine by valine in the pro alpha 1 (I) chain of type I procollagen.

The features of three babies with perinatal lethal osteogenesis imperfecta (OI II) resulting from substitutions of glycine by valine in the triple helical domain of the alpha 1(I) chain of type I collagen were studied. The babies were heterozygous for this substitution at residue 1006 in case 1 (OI35), 973 in case 2 (OI59), and 256 in case 3 (OI7B). OI35 had the most severe clinical form, OI IIC, with premature rupture of membranes, severe antepartum haemorrhage, stillbirth, severe short limbed dwarfism, and extreme osteoporosis. OI59 was a better formed baby but was also born prematurely as a result of premature rupture of membranes and severe antepartum haemorrhage. She had the radiographic features of OI IIA. OI7B was born at term and also had the radiographic features of OI IIA. Pathological examination of the skeletons of OI35 and OI59 showed grossly deficient intramembranous and endochondral ossification. Trabecular bone was sparse in the long bones and vertebrae. The trabeculae contained a cartilage core and an overlying layer of woven bone or osteoid. The diaphyses lacked cortical bone. The periosteal fibroblasts of OI35 contained grossly distended rough endoplasmic reticulum consistent with the 53% reduction in collagen secretion by cultured dermal fibroblasts. The aorta, skin, and lungs were hypoplastic in OI35 and OI59. The findings in this study show that glycine substitutions by valine in Gly-X-Y triplets, from glycine 256 to glycine 1006, of the triple helical domain of alpha 1(I) chains produce the OI II phenotype. The phenotype was most severe in the baby with the most carboxy-terminal substitution.

Adult↗

Maxillary giant cell reparative granuloma.

"Giant cell reparative granuloma" was introduced into medical literature by Jaffe in 1953. Prior to that time most authors considered this lesion to be a variant of the benign giant cell tumor of the long bones, or a giant cell variant of osteitis fibrosa. Bernier and Cahn established the subdivision between the rare central giant cell reparative granuloma and the common peripheral epulis. In the past, considerable emphasis has been placed on the importance of differentiating the true giant cell tumor from the giant cell reparative granuloma of the jaw bones. Most authors now believe the true giant cell tumor does not appear in the jaw bones except in rare cases associated with Paget's disease of the skull. Developing from membranous, rather than cartilaginous, ossification might account for this. Both peripheral and central intraosseous lesions, parathyroid osteopathy and the pathologic tissue of cherubism show no appreciable histologic difference. These tumefactions are histologically a proliferative fibroblastic lesion with multinucleated giant cells. The histopathology of the giant cell tumor of the long bones is probably identical to the histopathology of the giant cell reparative granuloma of the jaw bones. The diagnosis of giant cell reparative granuloma must be made by physical examination, history, laboratory, X-ray parameters and clinical follow-up. Localized maxillary swelling is the most important clinical feature. The swelling is smooth and palpation can reveal a rubbery, elastic sensation where bone has been thinned. There are no specific radiographic signs. Conservative surgical management is indicated and adequate for giant cell reparative granulomas. Radiation is not indicated because of long term risks. Steroids have not been proven useful.

Adult↗

[Osseous lesions in the elbow region in adolescents and adults (author's transl)].

Analysis of roentgenographs of injured elbows must go beyond the identification or exclusion of a line indicating a fracture, especially in children and adolescents. Decisive diagnostic pointers can be supplied by the displacement of fatty bodies, which is a very sensitive indicator of an intra-articular growth, as our postmortem examinations have shown. A systematic search for disturbances of relative positionings (which are defined e.g. by the radius-capitulum axis or the ventral longitudinal humerus axis) and consideration of the sequence in time of the appearance of ossification centres in elbows of children, will prevent gross mistakes in the assessment of the pathological situation.

Adolescent↗

[Gray scale histographic analysis of the acetabular cartilage for quantifying hip ultrasound images].

AIM: Congenital dislocated hips are classified in ultrasound studies using the angle measuring system of Graf and evaluating the typical changes in acetabular form and structure. We attempted to quantify physiological and pathological changes in the acetabular cartilage using B-mode scan ultrasound studies. METHODS: Gray-level histograms were performed on 894 infant hips; 833 were classified by the Graf scheme as Type IIa and 61 as Type IIIa/b. We compared the histological structure of the cartilage of both the acetabulum and the head of the femur using objective parameters. RESULTS: We could show that gray-level histograms of the acetabular cartilage are an ideal way to study objectively ultrasound evaluations of the same area. Type IIa hips with histographically identified ossification zones show significantly higher healing rates than those without such areas. Type IIIb hips with histographically demonstrated pathological changes showed a significantly longer healing rate and a higher incidence of persistent dislocations that did Type IIa hips with normal cartilage. CONCLUSION: Structural changes in the acetabular cartilage can be evaluated not only qualitatively but also quantitatively to provide prognostic information in infants with congenially dislocated hips. Gray-level histograms nicely supplement ultrasound examination.

Acetabulum↗

Idiopathic bilateral auricular ossificans: a case report and review of the literature.

Petrification of the auricle results in a rigid and immalleable ear. The etiology of such a finding is usually ectopic calcification. The condition has been associated with injurious processes, such as cold injury, and with various endocrinopathies, including Addison disease. In a significant number of cases, ossification occurs without knowledge of the precipitating cause or event. True auricular ossification is a rare occurrence, with only 12 histologically confirmed cases in the literature. We herein present the clinical and pathologic findings of another case. A 60-year-old man with diet-controlled diabetes presented with a 10-year history of slowly and insidiously stiffened auricles. He denied any precipitating historical events. Routine testing did not demonstrate systemic abnormalities. Radiographic examination revealed opacities consistent with bony structure in the auricles of the ears, with the right more prominent than the left. Histologic sampling demonstrated ossification with deposition of trabecular bone in proximity to normal elastic cartilage.

Ear Diseases↗