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At least 577 records · Page 32Linked to original sources
PubMed1994

Surgical treatment of ossification of the posterior longitudinal ligament in the thoracic spine.

Thoracic ossification of the posterior longitudinal ligament (OPLL) is a rare entity causing thoracic myelopathy. Its surgical decompression is still challenging. Three patients admitted with progressive myelopathy due to thoracic OPLL are described. A transthoracic anterolateral approach was used in the first and second cases, in which OPLL was located at the T3-T4 and T5-T6 and at the T7-T8 levels, respectively. In the third case, a transsternal approach was adopted for OPLL at the T1-T2 level. The OPLL, including dural ossification, was removed by microsurgical techniques as extensively as possible. Myelopathy in all three cases became relieved or stable postoperatively. Operative procedures are described in detail. From the viewpoint of surgical anatomy, the selection of operative approach depends on the level of the OPLL. The authors emphasize that a transthoracic anterolateral approach is the treatment of choice for extensive anterior pathology such as OPLL involving more than two thoracic bodies below the T4. A transsternal approach can provide excellent access to a lesion at the upper three thoracic bodies.

Aged↗
PubMedDate not supplied

Enalapril: pharmacokinetic/dynamic inferences for comparative developmental toxicity. A review.

Enalapril is an antihypertensive drug of the class of angiotensin-converting enzyme inhibitors (ACEI) used in pregnancy for treatment of pre-existing or pregnancy-induced hypertension. The use of ACE inhibitors (drugs that act directly on the renin-angiotensin system) during the second and third trimester of pregnancy in humans is associated with specific fetal and neonatal injury. The syndrome, termed "ACEI fetopathy" in humans, does not appear to have a similar counterpart in experimental animals. The present paper reviews pharmacokinetic and pharmacodynamic aspects of enalapril that are physiologically important during pregnancy and intrauterine development in humans and in experimental animal species with the aim of better understanding the comparability of the manifestations of enalapril developmental toxicity in animals and humans. The human fetus is at a disadvantage with regard to in utero enalapril exposure in comparison to some of the animal species for which gestational pharmacokinetic data are available. Important reasons for the higher vulnerability of the human fetus are its accessibility by enalapril and the earlier (relative to animal species) intrauterine development of organ systems that are specific targets of ACEI pharmacologic effect (the kidney and the renin-angiotensin system). In humans, these systems develop prior to calcarial ossification at the end of first trimester of pregnancy. The specific pharmacodynamic action of enalapril on these systems during fetal life is the chief determinant of the etiology and pathogenesis of ACEI fetopathy in humans. In contrast, in most of the studied animal species, these target systems are not developed until close to term when the fetus is relatively more mature (and therefore less vulnerable), so that the window of vulnerability is narrower in comparison to the human. Among animal species, the best concordance in fetal pharmacodynamics to the human is seen in the rhesus monkey, but further studies are necessary to determine if similar developmental pathology is induced in this animal model upon repeated administration of the drug during the relevant period of intrauterine development. Animal-human concordance of developmental toxicity is least likely in the rat because of greater disparities in enalapril availability to the fetus and the relative development of the kidney and skeletal ossification compared to that in humans.

Adult↗
PubMed2006

Ectopic ossification in the scar tissue of rats with myocardial infarction.

We describe the occurrence of bone-like formations in the left ventricular wall of infarcted rats treated or not with bone marrow cells injected systemically or locally into the myocardium. The incidence of ectopic calcification in hearts has been reported in rare cases in children with infarcts without previous coronary artery disease. Recently, ventricular calcification has been correlated with unselected bone marrow cell transplantation into infarcted rat hearts. Echocardiographic analysis of large infarction in rats frequently reveals the presence of echogenic structures in the left ventricular wall, sometimes projecting to the lumen of the chamber. The histological examination of these echogenic structures exhibited bone, cartilage, and marrow-like formations extending from the collagen-rich matrix of the ventricle wall. Microanalytical techniques verified the presence of hydroxyapatite in the mineral phase. Ossification was found in 25 out of 30 hearts evaluated 90 days postinfarct, being observed in 14 out of 17 animals submitted to cell therapy and in 11 out of 13 infarcted rats not submitted to cell therapy. Our study indicates that chondro-osteogenic differentiation can take place in the pathological rat heart independent of animal treatment with marrow cells.

Animals↗
PubMed1977

Case Report: epignathus-clinical, radiologic, and pathologic considerations.

In retrospect, a diagram could hace been made from the antenatal radiological examination of the case of epignathus presented here. The features of the epignathus are considered with respect to antenatal diagnosis and subsequent reparative surgery. Specific features such as axial organization, maturity of all tissues, and identical ossification points between host and parasite-all of which are evident in this case-favor the malformative origin of epignathi, thus distinguishing them from teratomata.

Abnormalities, Severe Teratoid↗
PubMed1977

[The role of glomi (arteriovenous anastomoses) in the pathomechanisms of solitary enchondromas (author's transl)].

The author performed the histlologic examination of 62 solitary enchondromas located in the short tubular bones of the hand and the feet. In 25 cases the thinned cortical bone and its periosteum covering the lesion could be examined, too. Comparison with the controls revealed that the glomi (arteriovenous anastomoses) in the periosteum, or close to it were open in 1 case, strongly contracted in 9 cases, and closed in 15 cases. It is shown throughout the whole material that the pathologic tissue of the enchondromas has a poor vascular supply. In 14 out of 62 cases the septa amoung the cartilaginous lobes were filled with blood. In the vicinity of these, however, a regular osteoblastic ossification sets in. The above results lead to the conclusion that in the pathomechanism of the enchondromas the local hypoxaemia induced by functional disturbance of the glomi plays an important role in the proliferation of the bradytrophic cartilaginous tissue.

Adolescent↗
PubMed2002

Bone abnormalities in latent TGF-[beta] binding protein (Ltbp)-3-null mice indicate a role for Ltbp-3 in modulating TGF-[beta] bioavailability.

The TGF-betas are multifunctional proteins whose activities are believed to be controlled by interaction with the latent TGF-beta binding proteins (LTBPs). In spite of substantial effort, the precise in vivo significance of this interaction remains unknown. To examine the role of the Ltbp-3, we made an Ltbp-3-null mutation in the mouse by gene targeting. Homozygous mutant animals develop cranio-facial malformations by day 10. At 2 mo, there is a pronounced rounding of the cranial vault, extension of the mandible beyond the maxilla, and kyphosis. Histological examination of the skulls from null animals revealed ossification of the synchondroses within 2 wk of birth, in contrast to the wild-type synchondroses, which never ossify. Between 6 and 9 mo of age, mutant animals also develop osteosclerosis and osteoarthritis. The pathological changes of the Ltbp-3-null mice are consistent with perturbed TGF-beta signaling in the skull and long bones. These observations give support to the notion that LTBP-3 is important for the control of TGF-beta action. Moreover, the results provide the first in vivo indication for a role of LTBP in modulating TGF-beta bioavailability.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Juvenile kyphosis in pigs. A spontaneous model of Scheuermann's kyphosis.

The development of kyphotic lesions in pigs with different weights from herds with a high frequency of the lesion was analysed pathologically, radiologically, and for alkaline phosphatase, calcium, magnesium, and phosphate in blood samples. The development of kyphosis was caused by the formation of ventral hemivertebrae due to the absence of ventral vertebral epiphyseal centres of ossification. Within the ventral parts of affected vertebral epiphyses, the retained chondroid tissue was dysplastic and the contents of cartilage canals with vessels often clotted with fibrin were reduced. As lesions such as fractures and inflammation that may be a secondary cause of kyphosis in pigs were absent and all blood parameters were within normal range, secondary causes of the condition, including metabolic disturbances, were excluded. It can be seen that the present type of porcine kyphosis does not develop until later in life as the ossification centres within the epiphyses of vertebrae have a retarded appearance. As the present porcine type of kyphosis pathomorphologically is comparable with Scheuermann's kyphosis in man, it constitutes a spontaneous model for this common cause of structural kyphosis of the thoracic or thoracolumbar spine.

Age Factors↗
PubMed1997

Paraplegia due to ossification of ligamenta flava in X-linked hypophosphatemia. A case report.

STUDY DESIGN: Spinal canal decompression at the most prominent of multiple posterior calcified thoracic lesions in a case of X-linked hypophosphatemia was undertaken for treatment and diagnosis purposes, as well as to assess possible nature of the pathophysiology underlying the presenting deficits. OBJECTIVES: To discuss the clinical assessment diagnostic and treatment aspects of this rare coincidence of ossification of ligamenta flava in the patient with the skeletal deformities of X-linked hypophosphatemia. SUMMARY OF BACKGROUND DATA: The patient with the stigmata and chemical findings of an X-linked hypophosphatemia presented with paraplegia and multiple calcified posterior spinal thoracic lesions. This was studied with magnetic resonance imaging and electrophysiologic studies of the spinal sensory pathways of the legs. These data constituted the preoperative information required to assess later results of surgical intervention. METHODS: Presurgical clinical, imaging and electrophysiologic studies and laboratory and pathologic investigations of the surgical specimens. RESULTS: Resolution of the paraplegia with walking and return to work in a physically demanding job for the last 4 or 5 years of postoperative follow-up after surgical decompression of the spinal cord only at the worst and highest of the effected spinal levels. CONCLUSION: The coincidence of X-linked hypophosphatemia and ossification of ligamenta flava has been reported only in two or three cases in the literature. Removal of the offending ossifying lesion is known to result in resolution of the clinical deficits but similar lesions at other spinal levels are suspected of producing recurrences. The return of function and of the corresponding electrophysiologic correlates indicate a neurono-apractic nature of the neurologic symptoms.

Bone and Bones↗
PubMed1988

Experimental microvascular autogenous vein grafts for arterial defects: II. A histopathologic study of the grafts.

Twelve autogenous vein grafts, of average diameter 1.5 mm, which had been used to bridge defects in the contralateral femoral artery of adult rabbits by a minimally traumatic technique, were examined over a 12-week postoperative period. Each graft remained widely patent but showed fibroelastic intimal thickening with time. Further evidence of arterialisation was the development of a prominent subintimal layer of smooth muscle. Also noted was the presence of medial fibrosis, with both calcification and ossification. This latter is suggestive of damage due to disruption of the vasa vasorum. It would appear that arterialisation of microvascular vein grafts occurs independently of surgical trauma and is therefore difficult to avoid. However, these pathologic changes were not as severe, nor was there as much luminal narrowing, as at the previously described anastomotic sites. The most important cause of these changes appears to be arterial pressure.

Animals↗
PubMed1991

Anterior ankle pain in sports medicine: aetiology and indications for arthroscopy.

Persistent pain and swelling in the anterior part of the upper ankle are encountered very frequently in sports traumatology. Classically, in the patient with a long history of typical anterior ankle pain there is no instability, but pinching effects, a sense of impingement, blocking and a feeling of unsteadiness combined with a certain restriction of movement due to the pathology. By analogy with the anatomical structures, various pathologic changes can lead to the classic clinical symptoms: adhesions, cicatrices, meniscoid-type lesions, osteophytes with synovitis, folds, fibrotic subcutaneous fatty tissue, free arthroliths, osteochondral lesions and arthrotic changes. When long-term conservative therapy has not provided a cure for the clinical syndrome surgical intervention becomes necessary. Arthroscopic interventions were carried out in a total of 21 patients, with follow-up times between 6 and 36 months. About two-thirds of all the patients showed good or very good results, while in one-third the results were unsatisfactory, mainly because of degenerative changes. An precise diagnosis is essential, but the significance of a pathologic change as the cause of symptoms can be problematical.

Ankle Injuries↗
PubMed1998

Type X collagen in the human invertebral disc: an indication of repair or remodelling?

The short-chained type X collagen was once thought to be produced exclusively by hypertrophic chondrocytes during endochondral ossification. More recently, however, it has been found elsewhere, for example in articular cartilage. In the present study, the occurrence of type X collagen in the intervertebral disc has been investigated. Human disc tissues of varying pathologies were examined for the presence of type X collagen and expression of alpha1(X) mRNA by immunohistochemistry and in situ hybridization respectively. All samples of disc contained areas that were immunoreactive but to varying extents. In the disc itself, staining for the protein and alpha1(X) mRNA was seen frequently associated with cells of the nucleus pulposus, which were large and of hypertrophic appearance, most commonly found in degenerate discs, and also in areas of disorganized architecture, such as clefts. In addition, type X collagen, both protein and mRNA, was found in regions of the cartilage end-plate, which calcify ectopically in scoliotic patients. We suggest that type X collagen production may be a response of disc tissue cells to a stimulus, such as altered loading.

Adolescent↗
PubMedDate not supplied

Prevalence of the Bennett lesion of the shoulder in major league pitchers.

BACKGROUND: The Bennett lesion is a mineralization of the posterior inferior glenoid noted in overhead throwing athletes. Although previous studies have debated appropriate treatment of the lesion, no studies have indicated the lesion prevalence in throwing athletes. HYPOTHESIS: The Bennett lesion is more common than previously believed and may represent an asymptomatic finding. STUDY DESIGN: Uncontrolled retrospective review. METHODS: Fifty-five asymptomatic major league pitchers underwent routine preseason radiographic screening. Radiographs were reviewed for the presence of a Bennett's lesion. Player demographics, pitching, and baseball records were reviewed to obtain the patient's dominant arm, age, years and innings pitched, and time on the disabled list or surgery. RESULTS: Twelve pitchers (22%) were noted to have a radiographic Bennett lesion. No statistically significant difference was noted in age, years pitched, or innings pitched between pitchers with and without a Bennett lesion. No player who demonstrated a Bennett lesion required surgical treatment for shoulder pain during his time with the club. Two players required time on the disabled list, but neither player had complaints of posterior shoulder pain. CONCLUSIONS: This lesion is a relatively common finding in major league pitchers. Concomitant pathology should be suspected when evaluating throwers with posterior shoulder pain and this lesion.

Adult↗
PubMedDate not supplied

The microscopic morphology of fluoride-induced bone.

To characterize further the bone changes in osteoporotic patients treated by a combined calcium, vitamin D, and sodium fluoride therapy regimen, full-thickness transilial undecalcified bone biopsy specimens from ten postmenopausal white women treated for idiopathic osteoporosis for 18-24 months were compared with those from ten age-, sex-, and race-matched untreated control subjects using standard light microscopy and histomorphometry. Statistically significant bone changes in the treated group consisted of cortical and trabecular new bone formation juxtaposed on underlying normal lamellar bone (p less than 0.001). The new bone showed increased osteocytic cellularity (p less than 0.001), irregular arrangement of osteocytes (p less than 0.001), enlarged osteocyte lacunae (p less than 0.001), and periosteocytic hematoxylinophilic staining intensity (p less than 0.001). Increases were also noted in trabecular bone volume (p less than .025), trabecular osteoid surface (p less than 0.001), and trabecular osteoid volume (p less than 0.001). Osteoid calculations were significantly less than those in the clinical and chemical osteomalacia observed in the authors' laboratory (p less than 0.01). Osteoclastic resorptive activity was increased (p less than .001), but no evidence of hyperparathyroidism was noted. These histologic and histomorphometric changes indicate accretion of new bone but with distinctly abnormal matrix characteristics. These are changes considered characteristic of the treatment and are pathologic markers of fluoride-induced abnormal bone formation.

Bone and Bones↗
PubMed1978

Effect of monosodium glutamate on the histogenesis of bone marrow in mice.

The effect of monosodium glutamate (MSG) on the histogenesis of bone and bone marrow of mice is studied. Intraperitoneal-subcutaneous injections and oral administration of the drug MSG induced marked repression in the ossification of developing endochondral bone with the persistence of cartilagenous elements and chondrocytes. A massive accumulation of adipose tissue accompanied by receded haemopoietic tissue within the bone marrow is observed in the MSG-treated animals. These pathological changes are attributed to the influence of the drug on the hydrolysis of enzyme alkaline phosphatase, glycolysis involved in the bone deposition or on the secretion of hormones responsible for bone resorption.

Administration, Oral↗
PubMed2004

[Vascular calcification].

Vascular calcification is a pathological calcification process. Its pathogenesis involves active mineralization by chondrogenic and osteogenic cells. Since cartilaginous metaplasia has been found in several vascular diseases, this process may represent one of vascular remodeling in response to vascular injury. Endochondral ossification following cartilaginous metaplasia play an important role in the progression of vascular calcification.

Animals↗
PubMed2001

Intellectual outcome of patients with congenital hypothyroidism detected by neonatal screening.

BACKGROUND AND PURPOSE: Mental retardation is a major sequela of delayed treatment for congenital hypothyroidism; congenital hypothyroidism can be treated early if detected with neonatal screening. We evaluated the intellectual outcomes of 62 patients with congenital hypothyroidism detected by neonatal screening at a major teaching hospital in northern Taiwan. The effects of thyroid pathology, age at the initiation of treatment, socioeconomic status, and severity of hypothyroidism on intellectual outcome were also analyzed. METHODS: All patients had euthyroid status at the time of intelligence testing. The Chinese Fourth Revision of the Binet-Simon Scales was used to evaluate the patients' intelligence between the ages of 3 and 6 years. RESULTS: The mean intelligence quotient (IQ) score was 102 +/- 18. Only four of the 62 patients were mentally retarded. Patients with lower initial serum thyroxine concentrations (T4; < 2 micrograms/dL) at the time of diagnosis of congenital hypothyroidism had significantly lower IQs (95 +/- 19, n = 26) than those with higher initial T4 concentrations (106 +/- 16, n = 36; p < 0.05). Patients with fewer than three ossification centers had lower IQs (91 +/- 20, n = 12) than those with three or more (104 +/- 17, n = 36; p < 0.05). Significantly lower IQs were also found in patients with a smaller femoral epiphysis area (< 0.1 cm2) (92 +/- 20, n = 15) than in those with larger epiphyses (106 +/- 15, n = 21; p < 0.05). The type of pathology (ectopia, athyrosis, dyshormonogenesis), age at the start of treatment (before or after 30 days of age), and socioeconomic status did not significantly affect the intellectual outcome. CONCLUSIONS: Our results indicate that intellectual outcome in Taiwanese patients with congenital hypothyroidism has been improved by neonatal screening and that the severity of hypothyroidism at diagnosis is the most important prognostic factor affecting intellectual outcome in these patients.

Age Factors↗