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PubMed1999

The relationship between facet joint osteoarthritis and disc degeneration of the lumbar spine: an MRI study.

The role of MRI in assessing facet joint osteoarthritis is unclear. By developing a grading system for severity of facet joint osteoarthritis on MRI, the relationship between disc degeneration and facet joint osteoarthritis was determined. The accuracy of MRI in assessing facet joint osteoarthritis against CT was 94%. Under 40 years of age, the degree of disc degeneration varied among individuals. Over the age of 60, most of the discs were markedly degenerated. Under 40 years of age osteoarthritic changes in facet joints were minimal. Over the age of 60, variable degrees of facet joint osteoarthritis were observed but some facets did not show osteoarthritis. No facet joint osteoarthritis was found in the absence of disc degeneration and most facet joint osteoarthritis appeared at the intervertebral levels with advanced disc degeneration. Disc degeneration is more closely associated with aging than with facet joint osteoarthritis. The present study supports the hypothesis that "disc degeneration precedes facet joint osteoarthritis", and also supports the concept that it may take 20 or more years to develop facet joint osteoarthritis following the onset of disc degeneration.

Adult↗
PubMed2006

Programmed cell death in intervertebral disc degeneration.

Intervertebral disc (IVD) degeneration is largely a process of destruction and failure of the extracellular matrix (ECM), and symptomatic IVD degeneration is thought to be one of the leading causes of morbidity or life quality deterioration in the elderly. To date, however, the mechanism of IVD degeneration is still not fully understood. Cellular loss from cell death in the process of IVD degeneration has long been confirmed and considered to contribute to ECM degradation, but the causes and the manners of IVD cell death remain unclear. Programmed cell death (PCD) is executed by an active cellular process and is extensively involved in many physiological and pathological processes, including embryonic development and human degenerative diseases. Thus, the relationship between PCD and IVD degeneration has become a new research focus of interest in recent years. By reviewing the available literature concentrated on PCD in IVD and discussing the methodology of detecting PCD in IVD cells, its inducing factors, the relationship of cell death to ECM degradation, and the potential therapy for IVD degeneration by modulation of PCD, we conclude that IVD cells undergo PCD via different signal transduction pathways in response to different stimuli, that PCD may play a role in the process of IVD degeneration, and that modulation of PCD might be a potential therapeutic strategy for IVD degeneration.

Animals↗
PubMed1990

Selective axonal and terminal degeneration in the chicken brainstem and cerebellum following exposure to bis(1-methylethyl)phosphorofluoridate (DFP).

Utilizing a variation of the Fink-Heimer method, we examined the extent and location of axonal and terminal degeneration within the chicken cervical spinal cord, brainstem and cerebellum resulting from a single subcutaneous dose of bis(1-methylethyl)phosphorofluoridate (DFP). The effects of DFP on the activities of whole-brain neuropathy target esterase (NTE) and cholinesterase (ChE) were also assessed as were the development and severity of clinical signs characteristic of organophosphorus-induced delayed neuropathy (OPIDN). Both whole brain NTE and ChE activities were maximally inhibited during the first 24 h post-exposure, showing gradual recovery over a period of 3 weeks. OPIDN clinical signs were not observed at 7 days post-DFP but progressed to severe ataxia by day 14 and paralysis by day 21. There was a relative absence of degeneration at 7 days, a dramatic increase in degeneration density at 14 days, and high density degeneration at both 21 and 28 days. Cervical spinal and medullary tracts containing axonal degeneration included the fasciculus gracilis, dorsal and ventral spinocerebellar tracts, spinal lemniscus, and the intramedullary portions of the glossopharyngeal and vagus nerves. Brainstem nuclei containing terminal degeneration included the lateral cervical, gracile-cuneate, external cuneate, and inferior olivary nuclei, the nucleus tractus solitarius, and the lateral and paragigantocellular lateral reticular nuclei. Mossy fiber degeneration was also present in cerebellar folia I-Vb. These results show that exposure to DFP causes axonal and terminal degeneration in ascending spinal tracts, brainstem nuclei and cerebellar folia associated with the transmission of somatic and visceral sensory information.

Animals↗
PubMed1997

Visual system degeneration induced by blast overpressure.

The effect of blast overpressure on visual system pathology was studied in 14 male Sprague-Dawley rats weighing 360-432 g. Blast overpressure was simulated using a compressed-air driven shock tube, with the aim of studying a range of overpressures causing sublethal injury. Neither control (unexposed) rats nor rats exposed to 83 kiloPascals (kPa) overpressure showed evidence of visual system pathology. Neurological injury to brain visual pathways was observed in male rats surviving blast overpressure exposures of 104-110 kPa and 129-173 kPa. Optic nerve fiber degeneration was ipsilateral to the blast pressure wave. The optic chiasm contained small numbers of degenerated fibers. Optic tract fiber degeneration was present bilaterally, but was predominantly ipsilateral. Optic tract fiber degeneration was followed to nuclear groups at the level of the midbrain, midbrain-diencephalic junction, and the thalamus where degenerated fibers arborized among the neurons of: (i) the superior colliculus, (ii) pretectal region, and (iii) the lateral geniculate body. The superior colliculus contained fiber degeneration localized principally to two superficial layers (i) the stratum opticum (layer III) and (ii) stratum cinereum (layer II). The pretectal area contained degenerated fibers which were widespread in (i) the nucleus of the optic tract, (ii) olivary pretectal nucleus, (iii) anterior pretectal nucleus, and (iv) the posterior pretectal nucleus. Degenerated fibers in the lateral geniculate body were not universally distributed. They appeared to arborize among neurons of the dorsal and ventral nuclei: the ventral lateral geniculate nucleus (parvocellular and magnocellular parts); and the dorsal lateral geniculate nucleus. The axonopathy observed in the central visual pathways and nuclei of the rat brain are consistent with the presence of blast overpressure induced injury to the retina. The orbital cavities of the human skull contain frontally-directed eyeballs for binocular vision. Humans looking directly into an oncoming blast wave place both eyes at risk. With bilateral visual system injury, neurological deficits may include loss or impairments of ocular movements, and of the pupillary and accommodation reflexes, retinal hemorrhages, scotomas, and general blindness. These findings suggest that the retina should be investigated for the presence of traumatic or ischemic cellular injury, hemorrhages, scotomas, and retinal detachment.

Air Pressure↗
PubMed2004

The compressive creep properties of normal and degenerated murine intervertebral discs.

Identifying mechanisms by which degeneration alters intervertebral disc material properties and biomechanical behavior is important for clarifying back pain risk factors as well as for evaluating the efficacy of novel interventions. Our goal was to quantify and characterize degeneration-dependent changes in the disc's response to compression using a previously established murine model of disc degeneration. We performed compressive creep tests on normal and degenerated murine intervertebral discs and parameterized the biomechanical response using a previously established fluid-transport model. Using a series of biochemical and histological assays, we sought to determine how biomechanical alterations were attributable to degeneration-related changes in tissue morphology. We observed that with moderate degeneration, discs lost height (mean+/-std. dev. of 0.44+/-0.01 vs. 0.36+/-0.01 mm, p<0.0001), increased in proteoglycan content (31+/-4 vs. 43+/-2 microg/ml of extract, p<0.0002), became less stiff (2.17+/-0.66 vs. 1.56+/-0.44 MPa, p<0.053), and crept more. Model results suggested that the increased creep response was mainly due to a diminished strain-dependent nuclear swelling pressure. We also noted that the model-derived tissue properties varied with the applied load magnitude for both normal and degenerated discs. Overall, our data demonstrate that architectural remodeling stimulated by excessive loading diminishes the disc's ability to resist compression. These results are similar to degeneration-dependent changes reported for human discs.

Animals↗
PubMedDate not supplied

The relationship between disc degeneration and flexibility of the lumbar spine.

BACKGROUND CONTEXT: A relationship between degenerative changes of the intervertebral disc and biomechanical functions of the lumbar spine has been suggested. However, the exact relationship between the grade of disc degeneration and the flexibility of the motion segment is not known. PURPOSE: To investigate the relationship between degenerative grades of the intervertebral disc and three-dimensional (3-D) biomechanical characteristics of the motion segment under multidirectional loading conditions. STUDY DESIGN/SETTING: A biomechanical and imaging study of human cadaveric spinal motion segments. METHODS: One hundred fourteen lumbar motion segments from T12-L1 to L5-S1 taken from 47 fresh cadaver spines (average age at death, 68 years; range, 39 to 87 years) were used in this study. The severity of degeneration (grades I to V according to Thomson's system) was determined using magnetic resonance (MR) images and cryomicrotome sections. Pure unconstrained moments with dead weights were applied to the motion segments in six load steps. The directions of loading included flexion, extension, right and left axial rotation, and right and left lateral bending. RESULTS: When the MR images were graded, 2 segments had grade I disc degeneration; 45, grade II; 20, grade III; 26, grade IV; and 21, grade V. When the cryomicrotome sections were graded, 14 segments had grade I disc degeneration; 31, grade II; 22, grade III; 26, grade IV; and 21, grade V. Segments from the upper lumbar levels (T12-L1 to L3-4) tended to have greater rotational movement in flexion, extension, and axial rotation with disc degeneration up to grade IV, whereas the motion decreased when the disc degenerated to grade V. In the lower lumbar spine at L4-5 and L5-S1, motion in axial rotation and lateral bending was increased in grade III. CONCLUSIONS: These results suggest that kinematic properties of the lumbar spine are related to disc degeneration. Greater motion generally was found with disc degeneration, particularly in grades III and IV, in which radial tears of the annulus fibrosus are found. Disc space collapse and osteophyte formation as found in grade V resulted in stabilization of the motion segments.

Adult↗
PubMed1956

Electron microscopic and histochemical observations of muscle degeneration after tourniquet.

As an experimental model for the different forms of muscle degeneration, injury caused by 2 hours' ischemia has been studied from 20 minutes to 16 hours after release of the tourniquet. Discoid degeneration developed in stretched fibers by dissolution of the I bands (Z substances and actin). The discs represented the Q bands (A-H-A). In fibers which passively maintained contraction lengths during degeneration, the Z substances were dissolved, but the continuity of the fibrils was preserved, since the filaments are continuous over all sarcomeres under these conditions. Mitochondria and the tubules of the endoplasmic reticulum swelled, ruptured, and disintegrated. Granular degeneration developed in fibers where mitochondria were abundant. Unstretched degenerating fibers with few mitochondria gave a homogeneous or hyaline appearance. The different forms of degeneration therefore were dependent on the status of stretch and the fiber type. The extent of degeneration was not a function of time after ischemia, there being both nearly normal and severely damaged fibers at 20 minutes and 16 hours after the release of tourniquets. When degeneration occurred, however, the basic alterations were the same in all fibers; there was mitochondrial and reticular swelling, dissolution of the Z substances, and finally disintegration of the contractile material. Some damage developed in the sarcolemmas and capillaries. The mitochondrial disintegration was not linked with inactivation of the succinic dehydrogenase system.

Animals↗
PubMed1999

Isolation and characterization of Drosophila retinal degeneration B suppressors.

The Drosophila retinal degeneration B protein (RdgB) is a novel integral membrane phosphatidylinositol transfer protein required for photoreceptor cell viability and light response. We isolated one intragenic suppressor (rdgBsu100) and four autosomal suppressors of the hypomorphic rdgBKS222 retinal degeneration phenotype. The rdgBsu100 suppressor dramatically slowed rdgBKS222's photoreceptor degeneration without significantly improving the electroretinogram (ERG) light response. One autosomal recessive suppressor [su(rdgB)69] significantly slowed rdgBKS222 retinal degeneration and restored the ERG light response near to that of the wild type. Unlike all the previously characterized rdgB suppressors, the four new autosomal suppressors do not affect the ERG light response in rdgB+ flies. Only Su(rdgB)116 exhibited a mutant phenotype in a rdgB+ background, which was smaller R1-6 rhabdomeres. We also examined the extent to which two previously identified visual transduction mutations suppressed rdgB retinal degeneration. Absence of one of the light-activated calcium channels (trpCM) slowed the onset of rdgB-dependent degeneration. However, loss of protein kinase C (inaC209), which blocks photoreceptor cell deactivation, desensitization, and light adaptation, failed to suppress rdgB degeneration under normal light conditions. This demonstrates that TRP activity, but not INAC, is required for rapid rdgB-dependent degeneration.

Animals↗
PubMed1987

Facet joint orientation, facet and costovertebral joint osteoarthrosis, disc degeneration, vertebral body osteophytosis, and Schmorl's nodes in the thoracolumbar junctional region of cadaveric spines.

The disc degeneration in the thoracolumbar junctional region (T10-L1) of 37 male cadaveric spines was recorded with the use of discography. From 24 of these spines the facet joint orientation and degenerative findings of the facet and costovertebral joints, vertebral bodies (osteophytosis) and discs, and Schmorl's nodes were recorded directly from bones. At T11-12, the most common site for the transitional zone between thoracic and lumbar facet type, there was a marked variation in the orientation of facets. The occurrence of degenerative findings and Schmorl's nodes at the three levels in the region differed. At T10-11, disc degeneration, vertebral body osteophytosis, and Schmorl's nodes were most common (anterior degeneration). At T12-L1, facet and costovertebral joint degeneration were dominant (posterior degeneration). At T11-12, disc degeneration, vertebral body osteophytosis, Schmorl's nodes, and facet and costovertebral joint degeneration all occurred (anterior and posterior degeneration). The results point to a pathoanatomic association between degenerative changes and facet orientation.

Adult↗
PubMed2001

Effects of anulus fibrosus and experimentally degenerated nucleus pulposus on nerve root conduction velocity: relevance of previous experimental investigations using normal nucleus pulposus.

STUDY DESIGN: Nerve conduction velocity was measured in the pig cauda equina after local application of anulus fibrosus or in vitro/postmortem degenerated nucleus pulposus from the same pig. OBJECTIVES: To analyze the effects of anulus fibrosus and degenerated nucleus pulposus on nerve conduction velocity. SUMMARY OF BACKGROUND DATA: Previous studies on nucleus pulposus-induced effects on nerve roots have used normal, nondegenerated nucleus pulposus. Because both anulus fibrosus and degenerated nucleus pulposus are commonly seen in the clinical situation of disc herniation, the value of the previous work could be questioned. METHODS: Anulus fibrosus and nucleus pulposus were harvested using a retroperitoneal approach. The nucleus pulposus was degenerated artificially either by addition of sodium lactate with HCl added to form a pH of either 6.0 or 3.5 (in vitro degeneration), or by storing the nucleus pulposus at 4 C until a pH of 6.0 (postmortem degeneration) was reached. After epidural application, the nerve conduction velocity was determined at 7 days (anulus fibrosus) or 3 days (degenerated nucleus pulposus). RESULTS: Application of anulus fibrosus did not induce any reduction of nerve conduction velocity. In vitro and postmortem degenerated nucleus pulposus induced a reduction of nerve conduction velocity similar to that of normal nucleus pulposus. CONCLUSIONS: Although only nerve function and not pain was assessed, it seems likely that previous experiments using normal nucleus pulposus may be relevant for evaluating the pathophysiologic mechanisms behind the nucleus pulposus-induced nerve root injury, also in a clinical perspective.

Animals↗
PubMed2001

Localization of cathepsins D, K, and L in degenerated human intervertebral discs.

STUDY DESIGN: Localization of cathepsins D, K, and L in degenerated intervertebral discs was examined by immunohistochemistry. OBJECTIVES: To determine the involvement of cathepsins in the pathomechanism of intervertebral disc degeneration by monitoring the immunolocalization of cathepsins in degenerated intervertebral disc tissue. SUMMARY OF BACKGROUND DATA: Cathepsins D, K, and L are enzymes that contribute to the matrix destruction seen in the articular cartilage affected by osteoarthritis and rheumatoid arthritis. However, little is known about the contribution of these cathepsins to intervertebral disc degeneration. METHODS: Paraffin-embedded sections of degenerated intervertebral disc tissue collected at the time of surgery (13 discs from 12 patients) were immunohistochemically stained with antibodies for cathepsins D, K, and L. For further characterization of the stained cells, immunohistochemical detection of CD68 and TRAP staining were performed. RESULTS: Hematoxylin and eosin staining revealed obvious signs of degeneration in all sections. Cathepsins D and L were immunolocalized in disc fibrochondrocytes at various sites exhibiting degeneration. Cathepsins K were found in tartrate-resistant acid phosphatase-positive multinucleated cells, in particular near the cleft within the cartilaginous endplate. However, few cells were positive for these cathepsins in anulus fibrosus that maintained the lamellar structure of collagen fibers. CONCLUSIONS: Marked expression of cathepsins D and L was observed at the site of degeneration. Cathepsins D and K localized in tartrate-resistant acid phosphatase-positive multinucleated cells existed at the cleft between the cartilaginous endplate and vertebral body. The site-specific localization of these cathepsins suggests the association of these proteinases with endplate separation and disorganization of the anulus fibrosus in degenerative spinal disorders.

Adult↗
PubMed2002

Does the morphology of the iliolumbar ligament affect lumbosacral disc degeneration?

STUDY DESIGN: An anatomic study of the iliolumbar ligament was performed in association with lumbosacral disc degeneration. OBJECTIVES: To determine whether the morphology of the iliolumbar ligament contributes to lumbosacral disc degeneration. SUMMARY OF BACKGROUND DATA: There have been few reports concerning the clinical significance of the iliolumbar ligament. METHODS: We dissected 25 male and 27 female cadavers and measured the length and cross-sectional area of the anterior and posterior bands of the iliolumbar ligament. The specimens were classified into three groups based on the grade of L4-L5 and L5-S1 disc degeneration: the L4-L5 disc was more degenerated than the L5-S1 disc (group L), the L4-L5 disc was less degenerated than the L5-S1 disc (group S), and both discs were equally degenerated (group E). The results were statistically compared among the three groups. RESULTS: The length of the posterior bands and the summation of the length of the anterior and posterior bands were significantly shorter in group L than in group S, and the cross-sectional area of the posterior bands and the summation of the cross-sectional area of the anterior and posterior bands were significantly larger in group L than in groups S or E in the male cadaver specimens. CONCLUSION: If the iliolumbar ligaments (especially the posterior band of the ligament) of a male patient are short and have a large cross-sectional area, the lumbosacral junction can be stabilized by the ligaments, with the L5-S1 disc being protected from degeneration. The L4-L5 disc may be prone to degeneration.

Adult↗
PubMed2006

Feasibility of using a human nucleus pulposus cell line as a cell source in cell transplantation therapy for intervertebral disc degeneration.

STUDY DESIGN: Assessment of the potential use of an immortalized human nucleus pulposus cell line as an alternative cell source in cell transplantation therapy for intervertebral disc degeneration. OBJECTIVES: To evaluate the effect of transplanting the human nucleus pulposus cell line into a disc degeneration model in rabbits and to define whether it is capable of becoming an alternative cell source for cell transplantation therapy for disc degeneration. SUMMARY OF BACKGROUND DATA: Interest in cell transplantation therapy for disc degeneration has been growing for several years, and a range of different cell types have been examined as possible donor cells. In addition, the establishment of a novel cell line that possesses some of the major characteristics of a normal human nucleus pulposus cells has been reported. METHODS: Human nucleus pulposus cell line was established, and cells were transplanted into a rabbit disc degeneration model. At 4, 8, and 24 weeks after transplantation, inhibition of intervertebral disc degeneration was assessed by examining the disc height, macroscopic appearance, histologic findings, and immunohistochemistry. In addition, aggrecan, versican, and Type II collagen gene expression in the nucleus pulposus were measured semiquantitatively at the mRNA level. Furthermore, the survival of transplanted cells was examined using immunohistochemistry for Simian Virus 40 T antigen, and the presence of graft-versus-host reaction was assessed by immunohistochemistry for CD4 and CD58. RESULTS: The disc height was significantly greater in the transplanted group than in the degenerative group's disc from 4 weeks' posttransplantation. Macroscopically, the nucleus pulposus was absent and there was loss of disc height in the degenerative group at 24 weeks after transplantation, whereas the nucleus pulposus was preserved in the transplanted group. Histologic examination showed that the structure of the inner anulus fibrosus was significantly preserved in the transplanted group, and the boundary between the nucleus and anulus could be clearly visualized. Expression of mRNAs of the nucleus pulposus matrix, aggrecan, and Type II collagen was significantly greater in the transplanted group than in the degenerative group. This indicates that transplantation of human nucleus pulposus cell line helped to preserve the matrix of the nucleus pulposus. Thus, transplantation of a human nucleus pulposus cell line was shown to delay disc degeneration in this rabbit model. CONCLUSION: The human nucleus pulposus cell line may become an alternative cell source for cell transplantation therapy of intervertebral disc degeneration.

Adult↗
PubMed2006

What is intervertebral disc degeneration, and what causes it?

STUDY DESIGN: Review and reinterpretation of existing literature. OBJECTIVE: To suggest how intervertebral disc degeneration might be distinguished from the physiologic processes of growth, aging, healing, and adaptive remodeling. SUMMARY OF BACKGROUND DATA: The research literature concerning disc degeneration is particularly diverse, and there are no accepted definitions to guide biomedical research, or medicolegal practice. DEFINITIONS: The process of disc degeneration is an aberrant, cell-mediated response to progressive structural failure. A degenerate disc is one with structural failure combined with accelerated or advanced signs of aging. Early degenerative changes should refer to accelerated age-related changes in a structurally intact disc. Degenerative disc disease should be applied to a degenerate disc that is also painful. JUSTIFICATION: Structural defects such as endplate fracture, radial fissures, and herniation are easily detected, unambiguous markers of impaired disc function. They are not inevitable with age and are more closely related to pain than any other feature of aging discs. Structural failure is irreversible because adult discs have limited healing potential. It also progresses by physical and biologic mechanisms, and, therefore, is a suitable marker for a degenerative process. Biologic progression occurs because structural failure uncouples the local mechanical environment of disc cells from the overall loading of the disc, so that disc cell responses can be inappropriate or "aberrant." Animal models confirm that cell-mediated changes always follow structural failure caused by trauma. This definition of disc degeneration simplifies the issue of causality: excessive mechanical loading disrupts a disc's structure and precipitates a cascade of cell-mediated responses, leading to further disruption. Underlying causes of disc degeneration include genetic inheritance, age, inadequate metabolite transport, and loading history, all of which can weaken discs to such an extent that structural failure occurs during the activities of daily living. The other closely related definitions help to distinguish between degenerate and injured discs, and between discs that are and are not painful.

Animals↗
PubMed1980

Primary myxomatous degeneration of cardiac valves. Clinical, pathological, haemodynamic, and echocardiographic profile.

Four hundred and ninety-nine surgically excised valves were examined for pathological evidence of myxomatous degeneration. Thirty-six valves (7%) had myxomatous degeneration as a major pathological finding. Fourteen valves (3%) had significant myxomatous degeneration of the pars fibrosa, a finding which we define as "primary myxomatous degeneration". Echocardiographic findings and catheterisation results were correlated with the clinical course, surgical results, and follow-up in these 14 patients. Echocardiograms in 10 of the 11 patients who had them (91%) showed abnormalities suggesting the presence of primary myxomatous degeneration. Echocardiography was more helpful than angiography in diagnosis. The histological pattern of primary mitral myxomatous degeneration appears to be identical to that seen in patients with mitral valve prolapse and five of six patients with mitral lesions had echocardiographic evidence of prolapse. None of the patients with primary myxomatous degeneration of the aortic valve had syphilis of Marfan's syndrome. While the aetiology of primary myxomatous degeneration of cardiac valves is not known, a link to a more generalised disorder is suggested.

Adult↗
PubMed2000

Corticobasal degeneration: evaluation of cortical atrophy by means of hemispheric surface display generated with MR images.

PURPOSE: To determine the characteristics of cortical atrophy in corticobasal degeneration and Alzheimer disease by using a hemispheric surface display generated with magnetic resonance (MR) images. MATERIALS AND METHODS: The magnitude and extent of cortical atrophy were evaluated with MR hemispheric surface display and volumetric measurement in three groups: 17 patients with corticobasal degeneration, 17 matched patients with Alzheimer disease, and 17 matched healthy control subjects. RESULTS: The extent and magnitude of cortical atrophy were larger in the group with corticobasal degeneration than in the group with Alzheimer disease. The parasagittal and paracentral regions were significantly more atrophic in patients with corticobasal degeneration than in patients with Alzheimer disease (P <.05). The mean hemispheric-to-total intracranial volume ratios were significantly smaller in the patients with corticobasal degeneration (61%) and those with Alzheimer disease (64%) than in control subjects (69%). Asymmetry of hemispheric volume was significantly larger in the group with corticobasal degeneration than in the control group. CONCLUSION: The extent of cortical atrophy in corticobasal degeneration is more widespread than was previously thought. Parasagittal and paracentral atrophy is a distinctive feature of corticobasal degeneration and distinguishes it from Alzheimer disease.

Aged↗
PubMed1993

Testicular degeneration and spermatid retention in young male rats.

The incidence of spontaneous testicular atrophy and its morphological changes in relation to stage-specific spermatogenesis were investigated in young Crl:CD/BR male rats at 10-12 wk of age used as controls for toxicity screening during 1983-1990. The incidence of testicular degeneration was 2.5% (5/197) in control rats used for oral toxicity studies and 9.4% (31/327) in rats used for inhalation studies. The epididymal tubules of rats with testicular degeneration had exfoliated germ cells and low sperm density. The high incidence of testicular degeneration observed in the control rats used in inhalation studies may be related to the stress associated with immobilization in the restrainer during nose-only exposure conditions. The severity of testicular degeneration in the inhalation studies was mostly minimal. In these minimally affected testes, mature spermatids (step 19) were retained within normal-appearing germinal epithelium at spermatogenic stages IX-XIV. Also, eosinophilic globular bodies (EGBs) were formed with elongated or mature spermatids throughout all spermatogenic stages, but the general architecture of germinal epithelium was normal in appearance. By electron microscopy, EGBs were sequestered necrotic spermatids, and the germ cell degeneration was associated with cytoplasmic vacuolation of Sertoli cells. In moderate testicular degeneration, markedly decreased maturing spermatids (steps 15-19) and a slight depletion of round spermatids were observed in stages I-VIII. In severe testicular degeneration, seminiferous tubules were lined with 1-2 layers of round spermatids and spermatocytes with giant cell formation. The round spermatids served as a marker to identify spermatogenic stages (I-VIII) of the atrophic tubules. Also, in severe testicular degeneration, tubules in spermatogenic stages X-XIV had no elongated spermatids, and spermatocytes were exfoliated with occasional giant cell formation. Many seminiferous tubules were lined with only 1-2 layers of spermatocytes, and specific germ cell markers were not present.

Administration, Inhalation↗
PubMed2000

Synovial joint degeneration and the syndrome of osteoarthritis.

The adverse effects of osteoarthritis on the quality of life for tens of millions of people and on the costs of health care and economic productivity make it a major health problem that will increase in incidence and impact with the aging of the population. Although in most patients the cause of osteoarthritis remains unknown and no cure has been identified, appropriate diagnosis and treatment, including education of the patients, can minimize symptoms and help patients maintain active and productive lives. Accomplishing this aim requires that physicians have an understanding of the pathophysiology of joint degeneration and the relationships between joint degeneration and the clinical syndrome of osteoarthritis. Although much remains to be learned about the development and progression of the joint degeneration responsible for osteoarthritis, it is clear that the loss of articular cartilage results from disruption of the structural integrity of the articular cartilage coupled with or caused by an imbalance in the anabolic and catabolic activity of the tissue. The progression of joint degeneration varies considerably among patients. In some individuals the joint degenerates rapidly; in others the degenerative changes progress slowly over decades and in others the disease may remain stable. In rare patients, the joint degenerative changes spontaneously improve. Although joint degeneration is the underlying cause of the symptoms of osteoarthritis, including joint pain and loss of joint function, not all patients with joint degeneration have symptoms of osteoarthritis. Future therapeutic approaches may include disease-modifying drugs and surgical procedures that correct mechanical abnormalities, debride joints, and replace degenerated articular cartilage with implants that stimulate restoration of a cartilaginous joint surface. Development of methods to detect and monitor subtle changes in cartilage metabolism and identify the joint changes that precede loss of articular cartilage may make it possible to detect the earliest signs of osteoarthritis, when therapeutic interventions have the greatest potential for preventing progression of the disease.

Humans↗