Cartilaginous differentiation in peritoneal tissues: a report of two cases and a review of the literature.
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Two cases of cartilaginous differentiation of the peritoneum not associated with an intraabdominal malignancy are described. This is the first detailed report of cartilaginous metaplasia of the peritoneum. The patients were female, ages 53 (Patient 1) and 77 years (Patient 2). Prior medical histories were significant for a culdotomy (to drain pelvic abscesses associated with pelvic inflammatory disease) in Patient 1 and for an open abdominal surgery in Patient 2. The peritoneal lesions were incidental findings in both cases. In Patient 1, surgery was performed for a septated ovarian cyst; the other patient underwent surgery to relieve obstructive bowel symptoms. In Patient 1, multiple firm, white lesions ranging from 2.0 to 7.0 mm were present on the serosal surfaces and the mesenteries of the small and large bowel. In Patient 2, a single firm, white lesion measuring 2 cm in maximum dimension was removed from the mesentery of the ileum. Microscopically, the lesions consisted of small nodules of mature hyaline cartilage surrounded by nondescript fibrous tissue and covered by mesothelium. There was no foreign body giant cell reaction, inflammation, or other reactive changes in the surrounding adipose tissue. These may represent metaplastic lesions of the secondary mullerian system, or a unique peritoneal response to previous surgical manipulation. Alternatively, these may represent benign neoplastic lesions (chondroma) of the submesothelium. (+info)
Painful spastic hip dislocation: proximal femoral resection.
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The dislocated hip in a non-ambulatory child with spastic paresis tends to be a painful interference to sleep, sitting upright, and perineal care. Proximal femoral resection-interposition arthroplasty is one method of treatment for this condition. We reviewed eight hips, two bilateral cases, with a mean follow-up of 30 months. Clinical improvement was observed in all except one case, with respect to pain relief and sitting tolerance. Some proximal migration was observed in three cases, despite routine post-operative skeletal traction in all cases and careful soft tissue interposition. One case showed significant heterotopic ossification which restricted prolonged sitting. This patient needed some occasional medication for pain. (+info)
Idiopathic heterotopic ossification in the intensive care setting.
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Heterotopic ossification is characterised by the periarticular deposition of ectopic bone. It typically occurs after trauma, neurogenic injury, or congenital causes. Idiopathic heterotopic ossification has been rarely reported. A patient who developed idiopathic heterotopic ossification in the intensive care unit without any known predisposing conditions is presented. (+info)
Morphological influence of ascorbic acid deficiency on endochondral ossification in osteogenic disorder Shionogi rat.
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The influences of chronic deficiency of L-ascorbic acid (AsA) on the differentiation of osteo-chondrogenic cells and the process of endochondral ossification were examined in the mandibular condyle and the tibial epiphysis and metaphysis by using Osteogenic Disorder Shionogi (ODS) rats that bear an inborn deficiency of L-gulonolactone oxidase. Weanling male rats were kept on an AsA-free diet for up to 4 weeks, until the symptoms of scurvy became evident. The tibiae and condylar processes of scorbutic rats displayed undersized and distorted profiles with thin cortical and scanty cancellous bones. In these scorbutic bones, the osteoblasts showed characteristic expanded round profiles of rough endoplasmic reticulum, and lay on the bone surface where the osteoid layer was missing. Trabeculae formation was deadlocked, although calcification of the cartilage matrix proceeded in both types of bone. Scorbutic condylar cartilage showed severe disorganization of cell zones, such as unusual thickening of the calcification zone, whereas the tibial cartilage showed no particular alterations (except for a moderately decreased population of chondrocytes). In condylar cartilage, hypertrophic chondrocytes were encased in a thickened calcification zone, and groups of nonhypertrophic chondrocytes occasionally formed cell nests surrounded by a metachromatic matrix in the hypertrophic cell zone. These results indicate that during endochondral ossification, chronic AsA deficiency depresses osteoblast function and disturbs the differentiation pathway of chondrocytes. The influence of scurvy on mandibular condyle cartilage is different from that on articular and epiphyseal cartilage of the tibia, suggesting that AsA plays different roles in endochondral ossification in the mandibular condyle and long bones. (+info)
Intraocular osseous metaplasia. A clinico-pathological study.
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PURPOSE: To evaluate the clinico-pathologic features of intraocular osseous metaplasia. METHODS: Pathology specimens of enucleated eyes submitted to the ophthalmic pathology service at a tertiary eye-care referral center between January 1995 and June 1999 were studied for intraocular osseous metaplasia. Specific histopathologic features noted in specimens with osseous metaplasia were the presence of retinal detachment, gliosis, retinal pigment epithelial hyperplasia, drusen, epiretinal membrane, fibrovascular proliferation and inflammation. Immunohistochemistry using monoclonal antibody against glial fibrillary acidic protein was performed to assess the glial component within the membranes and the proliferative vitreoretinal mass. Clinical records were reviewed and correlated with histopathologic findings. RESULTS: Osseous metaplasiaS was noted in 8 of 151 (5.2%) eyes examined. Clinical diagnosis in these was phthisis bulbi, staphyloma, absolute glaucoma and microphthalmos. Enucleation was performed for relief of symptoms (in painful blind eyes) or for cosmesis, and in an eye inciting sympathetic ophthalmia. Retinal detachment, gliosis and retinal pigment epithelial hyperplasia were noted in all the cases. Drusen with calcification or ossification (5 of 8), fibrovascular proliferation in the vitreous (5 of 8) and active inflammation (4 of 8) were the other associated histologic features. Location of ossification was subretinal in 3 cases, preretinal (ora serrata) in 1 case and in both locations in 4 cases. The eyes with subretinal osseous metaplasia had associated calcified drusen, while preretinal ossification was seen within the fibrovascular membranes. CONCLUSION: Chronic retinal detachment, hyperplasia and transdifferentiation of retinal pigment epithelium appear to be a few of the prerequisites for intraocular osseous metaplasia. Ossification can occur at isolated subretinal and preretinal locations or can involve both. Though a larger study is required to postulate the chronology of events, in this small series, isolated subretinal ossification appears to be initiated by calcification and ossification of drusen, while in the pre-retinal region it is associated with vitreoretinal proliferation. (+info)
The osteopetrotic mutation toothless (tl) is a loss-of-function frameshift mutation in the rat Csf1 gene: Evidence of a crucial role for CSF-1 in osteoclastogenesis and endochondral ossification.
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The toothless (tl) mutation in the rat is a naturally occurring, autosomal recessive mutation resulting in a profound deficiency of bone-resorbing osteoclasts and peritoneal macrophages. The failure to resorb bone produces severe, unrelenting osteopetrosis, with a highly sclerotic skeleton, lack of marrow spaces, failure of tooth eruption, and other pathologies. Injections of CSF-1 improve some, but not all, of these. In this report we have used polymorphism mapping, sequencing, and expression studies to identify the genetic lesion in the tl rat. We found a 10-base insertion near the beginning of the open reading of the Csf1 gene that yields a truncated, nonfunctional protein and an early stop codon, thus rendering the tl rat CSF-1(null). All mutants were homozygous for the mutation and all carriers were heterozygous. No CSF-1 transcripts were identified in rat mRNA that would avoid the mutation via alternative splicing. The biology and actions of CSF-1 have been elucidated by many studies that use another naturally occurring mutation, the op mouse, in which a single base insertion also disrupts the reading frame. The op mouse has milder osteoclastopenia and osteopetrosis than the tl rat and recovers spontaneously over the first few months of life. Thus, the tl rat provides a second model in which the functions of CSF-1 can be studied. Understanding the similarities and differences in the phenotypes of these two models will be important to advancing our knowledge of the many actions of CSF-1. (+info)
Thoracic cord compression due to ossified hypertrophied ligamentum flavum.
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Ossified ligamentum flavum is increasingly appreciated as an important cause of thoracic myeloradiculopathy. Fifteen patients with age ranging from 30-61 years were studied. Fourteen presented with spastic paraparesis, and radiculopathy was the only complaint in one patient. Routine skiagrams and myelograms showed non-specific changes. Baseline CT and CT myelogram, however, documented the ossification of ligamentum flavum comprehensively. MRI was done in three patients. Multiple levels of the disease were seen in two cases. Four patients had ossified posterior longitudinal ligament. Thickened ligamentum flavum should be considered as an important cause of thoracic cord compression. (+info)
Activation of beta-catenin-LEF/TCF signal pathway in chondrocytes stimulates ectopic endochondral ossification.
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OBJECTIVE: Members of the Wnt signaling protein family are expressed during cartilage development and skeletogenesis, but their roles and mechanisms of action in those processes remain unclear. Recently, we found that beta-catenin-LEF/TCF-dependent Wnt signaling stimulates chondrocyte maturation and hypertrophy and extracellular matrix calcification in vitro, events normally associated with cartilage-to-bone transition during skeletogenesis. Thus, we tested here whether activation of this pathway promotes endochondral ossification. DESIGN: Chick chondrocytes were infected with avian retroviral expression vectors encoding constitutive-active (CA) or dominant-negative (DN) forms of LEF, which activate or block beta-catenin-dependent Wnt signaling respectively. These cells and companion uninfected control cells were seeded into type I collagen gels and transplanted intramuscularly into nude mice. The resulting ectopic tissue masses forming over time in vivo were subjected to histological and molecular biological analyses. RESULTS: Transplantation of chick chondrocytes induced de novo endochondral bone formation. In situ hybridization and RT-PCR using species-specific probes and primers showed that the ectopic cartilaginous tissue was avian and thus donor-derived, whereas the bone tissue was mouse and thus host-derived. CA-LEF-expressing ectopic tissue masses contained abundant bone and marrow, while DN-LEF-expressing masses contained little bone and lacked marrow. CONCLUSIONS: Activation of beta-catenin-LEF/TCF-dependent Wnt signaling accelerates chondrocyte maturation and replacement of cartilage by bone. (+info)