[The pathological significance of paraarticular ossifications after total hip replacements (author's transl)].
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The pathologic changes in the spinal cord of three autopsied cases associated with ossification of the posterior longitudinal ligament ( OPLL ) are reported. Compression of the spinal cord was marked at the level of the intervertebral disc, and the spinal cord was strikingly flattened antero-posteriorly. Intensive damage was seen in the gray matter as compared to the white matter. The white matter showed demyelination and axon loss with status spongiosus, which was more marked in the postero-lateral than in the anterior columns. The most seriously damaged parts of the spinal cord showed tissue necrosis and cavity formation which extended from the central parts of the gray matter to the ventral parts of the posterior columns. Adventitial fibrous thickening of the vein, hyaline degeneration of the walls of the arterioles, and compression of the anterior spinal vein were observed in the damaged regions. It was evident that secondary circulatory disturbance due to the compression produced by the ossification was of significance in the pathogenesis of the spinal cord damage. A tangle of peripheral nerves, ectopic and reactive, with Schwann cell proliferation was present in the posterior median fissure and the postero-lateral columns in one case. The spinal nerve roots that showed marked demyelination and axon loss were damaged by ossification at the places where the anterior nerve roots emerged from the spinal cord and where the roots penetrate the dura. There was ossification of the dura mater in all cases examined.
Ossification of the posterior longitudinal ligament is a human genetic disease in which pathological ectopic ossification of the spinal ligaments develops. This leads to myelopathy or radiculopathy due to compression of the spinal cord. In this study, we investigated the histological features of orthotopic ossification of the spinal ligaments of senile Zucker fatty rats. A remarkably high incidence of orthotopic ossification was observed mainly in the thoracic spinal ligaments as compared with controls. The histopathological findings were similar to those for ossification of the human posterior longitudinal ligament. Bone morphogenetic proteins and activins, which exert their effects by way of specific type-I and type-II serine/threonine kinase receptors, play important roles in the formation of bone and cartilage. In the spinal ligaments of Zucker fatty rats, bone morphogenetic protein receptors and activin receptors were immunohistochemically detected around the ossified foci in a manner similar to that previously shown for the ossified tissue from patients who had ossification of the posterior longitudinal ligament. Thus, bone morphogenetic proteins and activin receptors might play important roles in orthotopic ossification of the spinal ligaments of Zucker fatty rats as well as in ossification of the posterior longitudinal ligament of humans. In addition, bone morphogenetic protein-receptor-IA was expressed in the nonossified ligament, suggesting that the spinal ligaments, of the rats may have a predisposition to orthotopic ossification. In the controls, no expression of bone morphogenetic protein receptors or of activin receptors was observed. In conclusion, there is a great degree of similarity between orthotopic ossification of the spinal ligaments of Zucker fatty rats and ossification of the posterior longitudinal ligament of humans. Thus, the rats provide a useful animal model for the study of ossification of the human posterior longitudinal ligament.
STUDY DESIGN: A histopathologic examination of a specimen that showed hypertrophy of the posterior longitudinal ligament of the cervical spine. OBJECTIVES: To illustrate the possibility of hypertrophy of the posterior longitudinal ligament as a prodromal condition to ossification of the posterior longitudinal ligament. SUMMARY OF BACKGROUND DATA: Despite much study, the pathology of ossification of the posterior longitudinal ligament still remains unclear. Hypertrophic change often is seen in the part of the ossified ligament; however, there have been few histopathologic reports on hypertrophy of the posterior longitudinal ligament. Some reports have suggested that hypertrophy of the posterior longitudinal ligament is a prodrome of ossification of the posterior longitudinal ligament. METHODS: A 64-year-old man was admitted to the hospital because of gait disturbance and developed oliguria. In a plain radiograph, segmental ossification of the posterior longitudinal ligament was found at C4, C5, and C6. Computed tomograph myelogram revealed a soft tissue shadow, maximum 3.8 mm in diameter, on the dorsal side of the ossification of the posterior longitudinal ligament at C5 and C6. Magnetic resonance T1-weighted image (T1WI) showed an equivalent signal with the intervertebral disc on the dorsal side of ossification of the posterior longitudinal ligament. This lesion was enhanced with Gd-DTPA and confirmed as hypertrophy of the posterior longitudinal ligament. Cervical anterior decompression and fusion were performed using Yamaura's technique. The ossified and thickened lesion was elevated and removed en bloc. Then, hematoxylin-eosin and toluidine blue staining was performed to detect metachromasia. RESULTS: Macroscopic examination of the specimen revealed that soft tissue formation was connected with the C4-C5 intervertebral space and extended downward to C6-C7. Histopatholgically, collagen fibers were proliferating in the long-axis direction on both ventral and dorsal sides. This was surrounded by extended nucleus pulposus-like chondrocyte tissue, where endplate cartilage was detected around the C4 pedicle. Roux staining was low, and partial vascular and cellular infiltration was observed, although it was not marked. CONCLUSION: The herniated nucleus pulposus involving endplate cartilage from C4-C5 was limited to the superficial layer, and proliferation of nucleus pulposus-like chondrocytes occurred in the herniated tissue, where they might undergo a change in cell phenotype. The results of the present study support the hypothesis that hypertrophy of the posterior longitudinal ligament is a prodromal condition to ossification of the posterior longitudinal ligament.
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Mineralization is an essential requirement for normal skeletal development, but under certain pathological conditions organs like articular cartilage and cardiovascular tissue are prone to unwanted mineralization. Recent findings suggest that the mechanisms regulating skeletal mineralization may be similar to those regulating pathological mineralization. In general, three forms of cell-mediated mineralization are recognized in an organism: intramembranous ossification, endochondral ossification and pathological mineralization. This review summarizes recent work that tried to elucidate how cell-mediated mineralization is initiated and regulated. To explain mineralization, several theories have been proposed. One theory proposes that mineralization is initiated within matrix vesicles (MVs). A second, not mutually exclusive, theory proposes that phosphate induces apoptosis, and that apoptotic bodies nucleate crystals composed of calcium and phosphate. A third theory suggests that mineralization is mediated by certain non-collagenous proteins, which associate with the extracellular matrix. Regardless of the way mineralization is initiated, the organism also actively inhibits mineralization by specific proteins and removal of an inhibitor may also induce mineralization. Although many studies greatly contributed to a better understanding of the mechanisms regulating cell-mediated mineralization, many questions remain about the mechanisms that trigger cell-mediated mineralization and how this process is regulated. Further investigation is necessary to develop in the future novel therapeutic strategies to prevent pathological mineralization.
Anterior cervical spine surgery has come of age, as a golden route for treating anteriorly placed cervical compressions ranging from simple prolapsed disc to long segment pathologies like ossification of posterior longitudinal ligaments and cervical spondylotic myelopathy. Numerous technical modifications of the procedure are described. The role of stabilisation established for several pathologies, is still debateable in surgery for cervical disc. Bone is the ideal tissue for fusion. Hydroxyapetite implants are goods, but costly for our set up. Methylmethacrylate has a limited role in elderly patients with malignancy and a short life expectancy. Anterior cervical instrumentation has mushroomed over the last decade. Acceptable as methods of immediate stabilisation, the choice of the system varies with the surgeon. The authors use simple titanium plates with locking screws for the purpose.
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We present 22 cases with inter-sterno-costoclavicular ossification. Clinical and pathological findings show that abnormal ossification observed in this situation is due to non-suppurative chronic inflammation of the soft tissues around the sterno-costo-clavicular region such as the costo-clavicular ligament. We have classified X-ray findings into three stages according to the extent of the ossification; localized, generalized, and hyperostotic, and show that the disease progressed in this sequence. A considerable number of the patients showed abnormal X-ray findings in the spine or the sacro-iliac joint. Frequent association of pustulosis palmaris et plantaris was noted in this disease. Most of the cases were treated effectively with anti-inflammatory drugs, but a few cases required surgical resection of the ossified mass with the clavicle or the first rib in order to relieve the severe pain.
Intraocular ossification was investigated in a series of 20 eyes. Only 12 eyes were phthisical. The etiological factors were trauma, inflammation, glaucoma and massive intraocular gliosis. Bone tissue was of the compact and spongy type. A correlation was found between the intraocular ossification and retinal detachment, intraocular hemorrhage, intraocular neovascularization and uveitis.
Bone mineral density (BMD) has not been clearly determined in patients with ossification of the posterior longitudinal ligament (OPLL) in the cervical spine. BMD in patients with OPLL was measured in the third vertebral body in the lateral projection and in the distal part of the radius in the anteroposterior projection using dual-energy X-ray absorptiometry (DXA). Patients with OPLL had significantly higher BMD than healthy controls in both the lumbar spine and radius. Observing BMD by gender and age group, high BMD was recognized especially in female patients over 60 years of age. Significantly increased BMD was observed in patients with ankylosing spinal hyperostosis (ASH) in addition to OPLL. These findings suggest that patients with OPLL may tend to develop systemic hyperostosis, leading to the pathological ectopic ossification observed in OPLL.
STUDY DESIGN: A case of ossification on both sides of the ligamentum flavum in the cervicothoracic junction is described. OBJECTIVES: To review the pathology associated with ossification of the ligamentum flavum in the spine and its incidence at the cervicothoracic junction. SUMMARY OF BACKGROUND DATA: The literature on the common sites for ossification of the ligamentum flavum is reviewed. No report described ossification on the outer surface of the ligament presenting as ossification nodules on the medial side of the apophyseal joint. METHODS: The clinical, radiographic, and pathologic features associated with ossification of the ligamentum flavum are presented. The ossified ligament grew into nodular masses on both surfaces: posterolaterally on the medial surface of the apophyseal joint and anteromedially on the undersurface of the lamina. The masses were connected by a film of elastic fibers from the remnant ligamentum flavum. RESULTS: The symptoms and physical signs of cervical myelopathy improved after laminectomy and removal of the ossified ligament. There was no recurrence. CONCLUSION: The reported case adds to the literature on the pathology associated with ossification of the spinal ligaments.
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The purpose of this study was to investigate the mechanism of cell death in chondrocytes of the growth plate. In the degenerative chondrocyte zone of the growth plate, apoptotic chondrocytes were defeated by the in situ nick end labelling method, by DNA analysis in agarose gel, and by electron microscopy. The results of the in situ nick end labelling method and the occurrence of a ladder pattern of DNA in agarose gel analysis indicated the activation of endogenous endonucleases, resulting in DNA fragmentation. Electron micrographs showed the early morphological changes associated with apoptosis. This report presents both morphological and biochemical evidence for apoptosis in the terminal hypertrophic chondrocytes of the growth plate. These data suggest that apoptosis of degenerative chondrocytes may play an important role in the control of normal and pathological endochondral ossification.
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