SEARCH · PubMed Health

Results for “DEGENERATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 667 records · Page 37Linked to original sources

PubMed1994

Disc degeneration affects the multidirectional flexibility of the lumbar spine.

STUDY DESIGN: An in vitro biomechanical investigation using human lumbar cadaveric spine specimens was undertaken to determine any relationship between intervertebral disc degeneration and nonlinear multidirectional spinal flexibility. SUMMARY OF BACKGROUND DATA: Previous clinical and biomechanical studies have not established conclusively such a relationship. METHODS: Forty-seven discs from 12 whole lumbar spine specimens were studied under the application of flexion-extension, axial rotation, and lateral bending pure moments. Three flexibility parameters were defined (neutral zone (NZ), range of motion (ROM), and neutral zone ratio (NZR = NZ/ROM)) and correlated with the macroscopic and radiographic degeneration. RESULTS AND CONCLUSIONS: In flexion-extension, the ROM decreased and NZR increased with degeneration. In axial rotation, NZ and NZR increased with degeneration. In lateral bending, the ROM significantly decreased and the NZR increased with degeneration. In all three loading directions, the NZR increased, indicating greater joint laxity with degeneration.

Adult↗

PubMed2000

Motion in lumbar functional spine units during side bending and axial rotation moments depending on the degree of degeneration.

STUDY DESIGN: Human lumbar spine specimens were tested in axial rotation and side bending. Motion was related to the grade of degeneration. OBJECTIVES: To determine the degree to which degeneration with fissure formation in the disc affects axial rotation of the lumbar functional spine unit. SUMMARY OF BACKGROUND DATA: There is controversy in the literature regarding the influence of severe degeneration and fissures of the disc on the range of axial rotation. METHODS: Thirty-six lumbar spine specimens were tested in axial rotation and side bending, by applying pure moments in an unconstrained setting. The motion in 6 df was recorded by dial gauges. The grade of degeneration was established by the grading schemes of Nachemson, Thompson, Adams, and Mimura. RESULTS: A significant increase of axial rotation and lateral translation under torque was found. This increase mainly took place between Grade 3 according to the schemes of Nachemson, Thompson, and Adams (no fissure formation) and the higher grades of degeneration (defined by fissure formation). Reduced disc height was always associated with fissures. CONCLUSIONS: A reduced lumbar disc height in radiographs seems to be associated with fissure formation in the disc. In this case, the range axial rotation after torque is increased in comparison with cases with less degeneration.

Adult↗

PubMed2000

Disc degeneration: a human cadaveric study correlating magnetic resonance imaging and quantitative discomanometry.

STUDY DESIGN: This human cadaveric study evaluated disc degeneration of the lumbar spine using magnetic resonance imaging and quantitative discomanometry. OBJECTIVE: To determine if a correlation exists between magnetic resonance imaging and quantitative discomanometry in determining disc degeneration of the lumbar spine. SUMMARY OF BACKGROUND DATA: Several studies analyzing disc degeneration of the lumbar spine have compared magnetic resonance imaging with discography and discomanometry. The reported results are conflicting. No studies exist that compare magnetic resonance imaging and quantitative discomanometry in assessing the disc degeneration of the lumbar spine. METHODS: Three fresh human cadaveric thoracolumbar spine specimens (two T11-S1 and one L1-S1) that included a total of 19 discs were used. Spines were scanned with magnetic resonance imaging, and the scans were read by a neuroradiologist. Using the quantitative discomanometry technique, discs were injected with normal saline, and pressure-volume curves were collected and quantified with six parameters: intrinsic pressure, leakage pressure, initial slope, slope from 0.0 to 0.1 mL, maximum pressure, and volume at maximum pressure. Data analysis was performed using Spearman's Rank Correlation (Rho) statistic. RESULTS: Based on the results from 19 discs, an overall good correlation between magnetic resonance imaging scores and the six quantitative discomanometry parameters was demonstrated. With exception of the volume at maximum pressure, correlation coefficients ranged between 0.61 to 0.78 with a P < 0.05. CONCLUSIONS: Magnetic resonance imaging scores and quantitative discomanometry parameters correlated well in the assessment of disc degeneration of the lumbar spine. Quantitative discomanometry may be an important technique for evaluating early disc degeneration, especially tears of the anular fibers, which may be missed on magnetic resonance imaging.

Aged↗

PubMed2000

Does long-term compressive loading on the intervertebral disc cause degeneration?

STUDY DESIGN: Coil springs were stretched and attached to produce a compressive force across the lumbar intervertebral discs of dogs for up to 53 weeks. OBJECTIVE: To test the hypothesis that compressive forces applied to the intervertebral disc for a long period of time cause disc degeneration in vivo in a dog model. SUMMARY OF BACKGROUND DATA: It is a commonly held belief that high forces applied to the intervertebral disc, and to joints in general, play a role in causing degeneration. METHODS: Coil springs were stretched and attached to produce a compressive force across the lumbar intervertebral discs (L3/L4) of 12 dogs. After up to a year, the dogs were killed, and their lumbar spines were removed and radiographed. The L3/L4 disc and the controls (T13/L1 and L4/L5) were excised and examined for visible signs of degeneration. The discs then were assessed using immunohistochemical analysis and enzyme-linked immunosorbent assay. Disc chondrocytes also were assayed for apoptosis. RESULTS: No obvious signs of degeneration in the discs (L3/L4) that had been under compression for up to a year could be observed. There was no disc bulging, anular fissures, or disc space narrowing. Some changes were observed at the microscopic level, although no thickening of the endplate was apparent. The enzyme-linked immunosorbent assay analysis provided significant data for all three regions of the disc (nucleus, inner anulus, and outer anulus). When comparing the compressed disc (L3/L4) with either of the control discs (T13/L1 and L4/L5), in the compressed disc: 1) the nucleus contained less proteoglycan and more collagen I and II; 2) the inner anulus contained less proteoglycan and collagen I; and 3) the outer anulus contained more proteoglycan and less collagen I. The collagen II differences for the inner and outer anulus were not significant. CONCLUSION: Compression applied to the lumbar intervertebral discs of dogs for up to a year does not produce degeneration in any visible form. It does produce microscopic changes and numerical changes, however, in the amounts of proteoglycan and collagen in the nucleus, inner anulus, and outer anulus. The present results add no credence to the commonly held belief that high compressive forces play a causative role in disc degeneration.

Animals↗

PubMed2002

COL9A3 gene polymorphism and obesity in intervertebral disc degeneration of the lumbar spine: evidence of gene-environment interaction.

STUDY DESIGN: Cross-sectional. OBJECTIVES: To evaluate the interaction between the COL9A3 gene polymorphism and persistent obesity in relation to lumbar disc degeneration. SUMMARY OF BACKGROUND DATA: Obesity has been suggested to be a risk factor for disc degeneration. There is some indication for an association between collagen IX genes and lumbar disc disease characterized by sciatica. However, the interaction between those factors in their influences on the risk of disc degeneration has not been studied. METHODS: Blood samples from 135 middle-aged men who had undergone magnetic resonance imaging (MRI) of the lumbar spine were analyzed for the presence of an arginine to tryptophan change in the COL9A3 gene (Trp3 allele). The men represented three occupations: 41 were machine drivers, 42 were carpenters, and 52 were office workers. The discs L2/L3-L5/S1 were evaluated on MRI, using decreased signal intensity of the nucleus pulposus, posterior disc bulges, and decreased disc height as signs of disc degeneration. Based on self-reports on body height and weight currently and at the age of 25 years, obesity history was classified as no obesity, persistent obesity, and other. Rothman's synergy index was used as a measure of interaction between two factors. RESULTS: The Trp3 allele and persistent obesity acted synergistically to increase the risk of dark nucleus pulposus, posterior disc bulge, and decreased disc height at L4/L5; of multilevel posterior disc bulges; and of decreased disc height. From 45% to 71% of disc degeneration among persistently obese individuals with the Trp3 allele could be attributed to the synergism of these two factors. CONCLUSION: The effect of obesity on lumbar disc degeneration seems to be modified by the collagen IX gene polymorphism, so that people who carry the Trp3 allele are at increased risk if they are persistently obese.

Alleles↗

PubMed2003

Pathologic evidence of degeneration as a primary cause of rotator cuff tear.

Histopathologic, histochemical, and morphometric studies were done on 80 medial stumps of torn rotator cuff tendons to clarify the cause of tears. A high prevalence and diffuse distribution of degenerative changes were observed in the rotator cuff tendons including thinning and disorientation of collagen fibers, myxoid degeneration, hyaline degeneration, chondroid metaplasia, calcification, vascularproliferation, and fatty infiltration. No distinct inflammatory reaction was observed. Thinning and disorientation of collagen fibers, myxoid degeneration, and hyaline degeneration were seen in all cases. All changes except vascular proliferation and fatty infiltration were more pronounced in the middle to deep layers of the tendons than in the superficial layer. The collagen fibers were disoriented in the deep layer of the tendons, shown by microscopic image analysis. The frequency and distribution of thinning and disorientation of collagen fibers, myxoid degeneration, and hyaline degeneration suggest that these are early degenerative processes. Chondroid metaplasia and calcification may be chronic pathologic changes that occur after tearing regardless of the type of tear. Preexisting degenerative change in the middle and deep layers of the tendon in association with microtrauma seems to be the main cause of rotator cuff tears.

Adipose Tissue↗

PubMed2004

Mechanical conditions that accelerate intervertebral disc degeneration: overload versus immobilization.

STUDY DESIGN: A review of the literature on macromechanical factors that accelerate disc degeneration with particular focus on distinguishing the roles of immobilization and overloading. OBJECTIVE: This review examines evidence from the literature in the areas of biomechanics, epidemiology, animal models, and intervertebral disc physiology. The purpose is to examine: 1) what are the degeneration-related alterations in structural, material, and failure properties in the disc; and 2) evidence in the literature for causal relationships between mechanical loading and alterations in those structural and material properties that constitute disc degeneration. SUMMARY OF BACKGROUND DATA: It is widely assumed that the mechanical environment of the intervertebral disc at least in part determines its rate of degeneration. However, there are two plausible and contrasting theories as to the mechanical conditions that promote degeneration: 1) mechanical overload; and 2) reduced motion and loading. RESULTS: There are a greater number of studies addressing the "wear and tear" theory than the immobilization theory. Evidence is accumulating to support the notion that there is a "safe window" of tissue mechanical conditions in which the discs remain healthy. CONCLUSIONS: It is concluded that probably any abnormal loading conditions (including overload and immobilization) can produce tissue trauma and/or adaptive changes that may result in disc degeneration. Adverse mechanical conditions can be due to external forces, or may result from impaired neuromuscular control of the paraspinal and abdominal muscles. Future studies will need to evaluate additional unquantified interactions between biomechanics and factors such as genetics and behavioral responses to pain and disability.

Animals↗

PubMed2005

Cellular therapy for disc degeneration.

STUDY DESIGN: Review article regarding the developing field of cellular therapies for symptomatic disc degeneration. OBJECTIVE: To review the rationale and discuss the results of cellular strategies that have been proposed or investigated for disc degeneration. SUMMARY OF BACKGROUND DATA: Disc degeneration is a substantial clinical problem. Disc degeneration begins with a loss of disc cells and alterations in the extracellular matrix of the disc. One promising approach for this problem involves the use of cells transplanted to the degenerative disc to achieve functional tissue repair. METHODS: The rationale for using cellular therapy for disc degeneration is discussed. The basic science studies involving cellular transplantation to the disc are reviewed and future directions of this line of research are discussed. RESULTS: Although substantial work remains, the future of cellular therapies for symptomatic disc degeneration appears promising. CONCLUSION: Continued research is warranted to further define the optimal cell type, scaffolds, and adjuvants that will allow successful disc repair in human patients.

Animals↗

PubMed2006

Determinants of the progression in lumbar degeneration: a 5-year follow-up study of adult male monozygotic twins.

STUDY DESIGN: A 5-year follow-up study of exposure of discordant monozygotic twin pairs with repeated interviews and spine imaging. OBJECTIVE: The primary goals were to record changes in the degenerative signs over a 5-year interval and to estimate the effects of familial influences and suspected environmental risk factors on the speed of lumbar degeneration. SUMMARY OF BACKGROUND DATA: Traditionally, disc degeneration has been attributed to aging and environmental exposures; recently, a dominant effect of genetics has been revealed. Yet the etiopathogenesis of disc degeneration remains poorly understood and controversial despite being a primary target of diagnostic and therapeutic interventions. METHODS: Among 116 monozygotic twin pairs, which had been examined 5 years earlier, 75 pairs (150 men) were reexamined. They were imaged using the same MRI scanner and examination protocol as at baseline. The data were analyzed using statistical methods for longitudinal studies. RESULTS: Progression in disc height narrowing, disc bulging, osteophytosis, and fatty degeneration in the lumbar spine was seen in about 7% to 13% of the discs in 7% to 46% of subjects during 5-year follow-up. Few degenerative findings appear to reverse; few disc height measures increased, some anular tears were no longer visible, and bulging/herniation diminished. New anular tears (in axial view) were detected in 1.5%, disappeared in 2%, and were unchanged in 5.3% of discs; in the sagittal view, new high intensity zones findings were identified in 0.5%, were no longer apparent in 1.6%, and were unchanged in 7.1% of discs. There were no clear changes in upper endplates: in 2.1% of discs, the irregularity score increased and in 1.8% it decreased. Familial aggregation, reflecting genetic, and shared environmental influences, explained 47% to 66% of the variance in progression of degenerative signs on lumbar MRI, and resistance training and occupational physical loading together explained 2% to 10% of the progression in the degenerative signs in lumbar MRIs. CONCLUSIONS: Progression of disc height narrowing, bulging, osteophytes, and fatty degeneration was detected in about 10% or less of the T12-S1 discs. Development and disappearance of anular lesions were rarer. No clear changes were seen in endplate irregularities. The results also confirm that hereditary effects have a dominant role in the progression of disc degeneration and suggest that occupational lifting and leisure time resistance training have modest additional effects.

Adult↗

PubMed2006

Osteogenic protein-1 injection into a degenerated disc induces the restoration of disc height and structural changes in the rabbit anular puncture model.

STUDY DESIGN: In vivo study of the effect of injection of osteogenic protein-1 (OP-1) on a rabbit anular needle puncture model of intervertebral disc (IVD) degeneration. OBJECTIVE: To study radiographic, magnetic resonance imaging (MRI), biochemical, and histologic changes in the rabbit IVD after injection of OP-1 into the nucleus pulposus in a needle puncture disc degeneration model. SUMMARY OF THE BACKGROUND DATA: Growth factors, such as OP-1, have the ability to stimulate synthesis of proteoglycans and collagen in vitro. The in vivo injection of OP-1 into the normal rabbit IVD has increased disc height and proteoglycan content in the anulus fibrosus and nucleus pulposus. However, to our knowledge, no attempts have yet been made to determine the effects of these growth factors in an in vivo model of disc degeneration. METHODS: New Zealand adolescent white rabbits (n = 90, 8 for baseline evaluation, 82 at 8 times) received an anular puncture in 2 noncontiguous discs with an 18-gauge needle to induce disc degeneration. Four weeks later, either 5% lactose (10 microL) or OP-1 (100 microg in 10 microL 5% lactose) was injected into the center of the nucleus pulposus. The disc height was followed radiographically for up to 24 weeks after the injections. At the 2, 4, 8, 12, and 24-week times after the injection, rabbits were euthanized, and MRI of the harvested spinal columns was obtained to grade the degeneration. The discs injected with OP-1 or lactose and noninjected discs were subjected to biochemical and histologic analysis. The specimens at the 24-week time were limited to histologic evaluation. RESULTS: The anular puncture with a needle induced a consistent disc narrowing within 4 weeks. The injection of OP-1 induced a restoration of disc height at 6 weeks, which was sustained for the entire experimental period, up to 24 weeks after the injection. The injection of lactose alone did not change the course of disc narrowing over the same time. MRI grading score showed significant differences between the OP-1 and lactose groups at the 8, 12, and 24-week times, suggesting an increase in water content in the nucleus pulposus of the OP-1 group. The proteoglycan content of the nucleus pulposus and anulus fibrosus was significantly higher in the OP-1 group than in the control group. The degeneration grades of the punctured discs in the OP-1 group were significantly lower than those in the lactose group. CONCLUSION: The results of this study show the feasibility of restoring degenerative rabbit discs by a single injection of OP-1 into the nucleus pulposus. Importantly, the effects of the OP-1 injection on disc height were sustained for up to 24 weeks. The metabolic changes in the cells, following a single injection, might be sustained and, thus, induce long-term changes in disc structure. An efficacy study in large animals is required to show further that the intradiscal injection of OP-1, or bone morphogenetic proteins or growth factors with similar properties would be useful for the structural restoration of the IVD in humans.

Animals↗

PubMed1990

Early degeneration and sprouting at the rat neuromuscular junction following acrylamide administration.

Prolonged acrylamide administration produces motor nerve-terminal branch degeneration and impairs axonal outgrowth following nerve crush. It is unclear how early terminal branch degeneration is initiated and whether there is a compensatory regenerative response at the neuromuscular junction (NMJ). A modified Pestronk and Drachman silver-acetylcholinesterase strain was used to carry out a detailed morphometric analysis of the NMJ in soleus and lumbrical muscles. Rats were given 3, 5, or 10 doses of acrylamide, 35 mg/kg/day, by intraperitoneal injection, 5 days/week, and killed 4, 7, or 14 days after the first dose, respectively. Degenerating terminal branches were evident in soleus NMJ after only three doses of acrylamide. Diminished synaptic vesicle content, neurofilament accumulations and tubulo-vesicular profiles were evident after three doses. At later time points, degenerating terminals contained few synaptic vesicles and were engorged with neurofilaments. Endplate lengthening, indicative of denervation supersensitivity, accompanied degeneration. Terminal sprouting proliferated after 3 and 5 doses but was less prominent after 10 doses. Although similar changes occurred in the lumbrical muscle, they were not initiated until after 5 doses. These experiments reveal that pathological changes in terminal branches commence earlier and after a lower cumulative dose of acrylamide than previously reported and suggest that acrylamide exerts a primary effect at motor nerve-terminal branches. Early, vigorous terminal sprouting indicates that acrylamide does not prevent the initiation of regeneration, but with prolonged treatment does cause degeneration of maturing sprouts.

Acrylamide↗

PubMed1989

The non-invasive investigation of lumbar disc degeneration in patients with chronic low back pain.

The painful degenerate disc is a recognised cause of low back pain. Magnetic Resonance Imaging (MRI) has now replaced discography in the non-invasive assessment of disc degeneration. However, the prohibitive capital expense of MRI and the small number of MR units in Australia produce limitations in clinical access. In contrast, Computed Tomography (CT) is readily available and is performed in most patients prior to MRI referral. This prospective study was undertaken to determine whether preliminary CT could offer any information about disc degeneration and so reduce the demand on a MRI scanner. 30 consecutive patients were studied all of whom had both CT and MRI examinations. Of a total 107 discs examined by both techniques, MRI was able to identify 37 degenerate discs. Conclusive evidence of degeneration (i.e. the presence of intervertebral gas) was only seen in 3 discs at CT (1 patient). Of the 29 posterior disc bulges found on CT, all were both bulging and degenerate on MRI. Indications for MRI based on the CT findings are recommended. Using these criteria, 13% (4 patients) of this study group could have avoided an expensive and unnecessary MR investigation. A useful algorithm for the investigation and assessment of patients with chronic low back pain is discussed.

Adult↗

PubMed2005

Presenile dementia mimicking Pick's disease: an autopsy case of localized amygdala degeneration with character change and emotional disorder.

This report concerns an autopsy case showing localized amygdala degeneration. The patient was a Japanese single woman without hereditary burden who was 58 years old at the time of death. At the age of 55 years, the patient began to feel anxiety, agitation and depressive in mood. At age 58 years, she developed marked character changes and emotional disorders, although disorientation and memory disturbance were slight. We suspected her disease was a variant of presenile dementia, especially Pick's disease, and some neuroradiological examinations disclosed bilateral temporal involvements. We could not make a definitive diagnosis from the clinical findings. She choked to death 3 years after the disease onset. From the neuropathological examinations, the known neurodegenerative diseases causing dementia, including Pick's disease, were excluded and we diagnosed our case as having localized amygdala degeneration. Localized amygdala degeneration itself is very rare. Moreover, in this case, the amygdala degeneration was presumed to be idiopathic, without any apparent cause. To our knowledge, this is the first case of idiopathic localized amygdala degeneration. This case indicates that localized amygdala degeneration can cause presenile dementia, and that character changes and emotional disorders are predominant over memory disturbance and/or disorientation.

Affective Symptoms↗

PubMed1990

Evidence that the Rate of Wallerian Degeneration is Controlled by a Single Autosomal Dominant Gene.

In a substrain of C57BL mice, C57BL/Ola, Wallerian degeneration in the distal segment of the severed sciatic nerve is extremely slow when compared to other mice. Despite this very slow degeneration in the distal segment regeneration of the motor nerves is not impaired. From suitable genetic outcrosses and backcrosses, the authors provide evidence that the rate of Wallerian degeneration in this strain is controlled by a single autosomal gene product. The authors have also shown that the rate of degeneration, in C57BL/Ola mice, is influenced by the environment in which the animals were bred and housed. Wallerian degeneration in the sciatic nerves of mice raised in isolators is slower than in those raised in a conventional animal house. This strain of mouse may prove to be of value in the understanding of nerve degeneration and regeneration.

Journal Article↗

PubMed2005

beta-Catenin expression during vascular development and degeneration of avian mesonephros.

beta-Catenin is a structural component of adherens junctions, a regulator of the Wnt signalling pathway and a transcriptional co-activator with a key role in vascular patterning. The avian mesonephros is a transitory embryonic kidney that is used in the study of vascular development and degeneration. Here we examine beta-catenin expression in this model during vascular development and degeneration. Quail embryos with developing or degenerating mesonephros were studied, on day 6 (30HH) or day 11 of incubation (40HH), respectively. QH1 whole mounts of developing mesonephros revealed numerous angioblast-like cells situated in the paramesonephric duct that seem to invade the mesonephros. Although these cells did not express beta-catenin, the surrounding periductal mesenchymal cells translocated high levels of beta-catenin into the nucleus. In contrast, degenerating mesonephros were devoid of angioblast-like cells and beta-catenin was lower than in the developing mesonephros. beta-Catenin was significantly reduced in the glomerular capillary tuffs, indicating that it was particularly down-regulated in the vascular system. No sex-related differences in beta-catenin expression were observed in degenerating mesonephros. Furthermore, two special populations of glomerular and peritubular endothelial cells were observed in degenerating mesonephros: one translocating beta-catenin into the nucleus and the other in apoptosis that did not translocate it. In conclusion, our results indicate that the paramesonephric duct is a potential new vasculogenetic pathway, and suggest that beta-catenin plays a role in the fate of mesonephric endothelial cells.

Animals↗

PubMed2006

Potential outcome factors in subacute combined degeneration: review of observational studies.

BACKGROUND: Subacute combined degeneration is an acquired myelopathy caused by vitamin B12 deficiency. Therapy with B12 leads to improvement in most but to complete recovery in only a few patients. Prognostic indicators in subacute combined degeneration are unknown; therefore, predicting complete recovery of neurologic deficits is challenging. PURPOSE: To identify potential correlates of outcome and to generate hypotheses concerning predictors of complete resolution of neurologic deficits in subacute combined degeneration. DATA SOURCE: We searched EMBASE (1974 to October 2005), MEDLINE (1968 to October 2005), and references from identified reports. REPORTS SELECTION: Reports of patients with subacute combined degeneration containing results of magnetic resonance imaging (MRI) and description of outcome and 1 patient treated by the authors. DATA EXTRACTION, SYNTHESIS: We extracted data from 45 reports and 57 patients (36 males, 21 females; age range: 10 to 81) with a diagnosis of subacute combined degeneration, and estimated the strength of association between clinical, laboratory, and radiological factors and complete resolution of signs and symptoms. RESULTS: Eight patients (14%) achieved clinical resolution and 49 (86%) improved with B12 therapy. The absence of sensory dermatomal deficit, Romberg, and Babinski signs were associated with a higher complete resolution rate. Patients with MRI lesions in < or = 7 segments and age less than 50 also appear to have higher rates of complete resolution. CONCLUSIONS: B12 therapy is reported to stop progression and improve neurologic deficits in most patients with subacute combined degeneration. However, complete resolution only occurs in a small percentage of patients and appears to be associated with factors suggestive of less severe disease at the time of diagnosis.

Adolescent↗

PubMed2005

Influence of cervical disc degeneration after posterior surgical techniques in combined flexion-extension--a nonlinear analytical study.

Laminectomy and facetectomy are surgical techniques used for decompression of the cervical spinal stenosis. Recent in vitro and finite element studies have shown significant cervical spinal instability after performing these surgical techniques. However, the influence of degenerated cervical disk on the biomechanical responses of the cervical spine after these surgical techniques remains unknown. Therefore, a three-dimensional nonlinear finite element model of the human cervical spine (C2-C7) was created. Two types of disk degeneration grades were simulated. For each grade of disk degeneration, the intact as well as the two surgically altered models simulating C5 laminectomy with or without C5-C6 total facetectomies were exercised under flexion and extension. Intersegmental rotational motions, internal disk annulus, cancellous and cortical bone stresses were obtained and compared to the normal intact model. Results showed that the cervical rotational motion decreases with progressive disk degeneration. Decreases in the rotational motion due to disk degeneration were accompanied by higher cancellous and cortical bone stress. The surgically altered model showed significant increases in the rotational motions after laminectomies and facetectomies when compared to the intact model. However, the percentage increases in the rotational motions after various surgical techniques were reduced with progressive disk degeneration.

Biomechanical Phenomena↗

PubMed1996

Prevalence and possible pathological significance of calcium phosphate salt accumulation in tendon matrix degeneration.

OBJECTIVES: To investigate the prevalence of calcium phosphate mineral salt accumulation in degenerative supraspinatus 'tendinitis' compared with a normal sample of human tendons, and to determine whether there is an association of calcium salt deposition with pathological changes in the tendon extracellular matrix. METHODS: Cadaver tendons (supraspinatus and common biceps tendons, n = 96) and fragments of supraspinatus tendons obtained during shoulder surgery (n = 31) were analysed for calcium content by atomic absorption spectroscopy, phosphorous content using a spectrophotometric assay, and matrix composition (collagen, glycosaminoglycans and DNA) using standard biochemical techniques. RESULTS: We established baseline values of calcium concentration in macroscopically normal cadaver tendons (mean 1.1 (SD 0.35) micrograms/mg dry wt, n = 60) and found that 33% (nine of 27) of ruptured tendons from patients with 'degenerative tendinitis' contained an excess of calcium (more than 2SD greater than the normal sample mean). Five of these specimens had increased concentrations of phosphorous and calcium:phosphorous (molar) ratios consistent with a variety of possible calcium crystals, including calcium pyrophosphate, hydroxyapatite, and tricalcium phosphate, in addition to mixed or amorphous calcium phosphate deposits. Four of these specimens contained normal concentrations of phosphorous, consistent with deposits of calcium oxalate or calcium carbonate, although this was not confirmed biochemically. In contrast, surgical specimens (n = 4) from patients with 'calcifying tendinitis' (radiographically detected calcium deposits) all contained salts with a mineral composition consistent with hydroxyapatite. The presence and identity of crystal deposits was subsequently confirmed in five specimens by radiographic microanalysis. Analysis of the tendon matrix demonstrated a number of significant differences between normal and degenerate (ruptured) tendons, including a reduction in collagen content, an increase in sulphated glycosaminoglycans (predominantly dermatan sulphate) and an increase in DNA (cellular) content. However, there were no significant differences between degenerate tendons that were 'calcified' and those degenerate specimens that contained normal concentrations of calcium. CONCLUSIONS: Although there was a relatively high prevalence of calcium salts in degenerate tendons, which might contribute to the pathological process (such as increased matrix collagen degradation), these data are consistent with the hypothesis that 'dystrophic calcification' of degenerate tendon matrix is a pathological entity distinct from cell mediated 'calcifying tendinitis'. Calcification is probably one possible outcome (or end point) of chronic tendon injury, although the possibility exists that in many cases, the presence of calcium salts may contribute to the tendon matrix degeneration.

Adolescent↗