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.

The effect of compressive force applied to the intervertebral disc in vivo. A study of proteoglycans and collagen.

STUDY DESIGN: Coil springs were stretched and attached to produce a compressive force across the lumbar intervertebral discs of dogs for up to 27 weeks. OBJECTIVE: To test the hypothesis that a high compressive force applied over a period of time affects the production of proteoglycans and collagen by the intervertebral disc cells. 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: Pairs of stainless steel coil springs were stretched and attached to produce a compressive force across the lumbar intervertebral discs (L1-L2 and L3-L4) of 16 dogs. Dogs were killed between 13 and 27 weeks after the springs were attached. The discs (L1-L2 and L3-L4) were excised and assessed using immunohistochemical analyses and enzyme-linked immunosorbent assay; T13-L1 and L4-L5 were used as controls. RESULTS: The main result relates to a group effect in the six dogs, assessed using enzyme-linked immunosorbent assay, that were generally at the highest values of force for the greatest number of weeks. For the nucleus, but not the anulus, Spearman rank correlations revealed a strong correlation between increases in force and force-weeks (force multiplied by number of weeks) and increases in collagen type I accompanied by decreases in proteoglycans, chondroitin sulfate, and collagen type II for both experimental discs (L1-L2 and L3-L4), as compared with corresponding values in the controls (T13-L1 and L4-L5). In other words, as either the force or the force-weeks increased, the effect on the nucleus became greater. CONCLUSION: A high compressive force applied to the disc over a period of time initiates changes in proteoglycans and collagen.

The compartments of the hand: an anatomic study.

To determine the nature and number of enclosed myofascial spaces in the hand, an anatomic study that included 21 cadaver hands was conducted using a gelatin injection method. Data were collected from the prepared cross-sections of each specimen. The results showed the thenar space to comprise 2 or more discrete compartments in 52% of the hands. In 76% of the specimens, the hypothenar space demonstrated at least 2 compartments. The adductor pollicis and first dorsal interosseous muscles were discrete compartments in 71% of the hands. The interosseous compartments demonstrated significant variability. The dorsal and palmar interosseous muscles were discrete compartments within the second interosseous compartment in 48% of the hands, within the third interosseous compartment in 67%, and within the fourth interosseous compartment in 33%. Subcompartmentalization of the enclosed myofascial spaces of the hand should be anticipated in cases requiring fasciotomy. Thorough inspection within anatomic areas or generous release of the muscular origin along the metacarpal at the time of fasciotomy is suggested to ensure complete inspection.

Reversing the inhibitory effect of nicotine on spinal fusion using an osteoinductive protein extract.

STUDY DESIGN: The effect on spinal fusion of an osteoinductive bone protein extract in the presence of a known inhibitor of spinal fusion (systemic nicotine) was studied prospectively in an animal model of posterolateral lumbar fusion. OBJECTIVES: To evaluate the ability of a bovine-derived osteoinductive bone protein extract to overcome the inhibitory effect of nicotine in a rabbit spine fusion model. SUMMARY OF BACKGROUND DATA: Multiple studies have demonstrated the ability of a variety of osteoinductive growth factors to serve as a bone graft substitute for lumbar spinal fusion under "normal" healing conditions. METHODS: Forty-eight adult female New Zealand white rabbits underwent spine arthrodesis at L5-L6 while receiving systemic nicotine through a subcutaneous miniosmotic pump. Arthrodesis was performed using one of the following three graft materials: 1) autogenous iliac crest, 2) osteoinductive bone protein delivered in an allogeneic demineralized bone matrix/ collagen carrier, or 3) osteoinductive bone protein delivered with autogenous iliac crest. Fusions were assessed by blinded manual palpation, radiography, and biomechanical testing. RESULTS: Of the 44 rabbits manually tested by blinded observers, all 14 in the osteoinductive bone protein plus autogenous iliac crest bone group had solid fusions (14 of 14), whereas the fusion rate was less in the osteoinductive bone protein plus demineralized bone matrix group (nine of 14, 64%; P = 0.02), and there were no fusions in the autogenous iliac crest only group (0 of 16, 0%; P = 0.000001). The use of osteoinductive bone protein with autogenous bone produced stronger and stiffer fusions compared with those using autogenous bone alone or osteoinductive bone protein with allograft bone. CONCLUSIONS: Cigarette smoking and nicotine are inhibitory factors in the healing of fractures and spine fusions. This study shows that the inhibitory effect of nicotine can be overcome with an osteoinductive bone growth factor in an animal model.

The effect of nicotine on incorporation of cancellous bone graft in an animal model.

STUDY DESIGN: A basic science study using a rabbit model of bone graft revascularization in the distal femoral metaphysis. OBJECTIVES: The goal of the present study was to determine the effect of nicotine on the revascularization and incorporation of autogenous iliac crest bone graft implanted in an orthotopic location. SUMMARY OF BACKGROUND DATA: Although nicotine is the major toxin in cigarettes, it has not been confirmed as the primary factor affecting bone metabolism, and although the effects of smoking on bone homeostasis have been well studied, the effect of nicotine on new bone formation and neovascularization in the setting of bone graft transplantation has not been well studied. METHODS: Twenty-four New Zealand white rabbits were randomly divided into two groups to be exposed to nicotine or saline control. A cancellous iliac crest bone graft was harvested and implanted in the lateral distal femur. Mini-osmotic pumps were used to deliver continuous serum levels of nicotine. The animals were killed at the following intervals: 1 week (n = 6), 2 weeks (n = 12), and 4 weeks (n = 6). The vascular tree was injected with Microfil silicone rubber solution, and the degree of revascularization was determined with a semiautomated image analysis system to determine the area of vascularization for each specimen. RESULTS: All seven of the control (no nicotine) animals harvested at 1 or 2 weeks had over 50% bony vascular ingrowth, whereas only four of the nine nicotine-exposed animals showed over 50% bony vascular ingrowth. These differences were statistically significant (P = 0.03) using the Fischer exact test. By the fourth week (after nicotine levels in experimental animals had diminished), the revascularization of the nicotine-exposed grafts was indistinguishable from that of grafts in the animals that were not exposed to nicotine. CONCLUSIONS: We conclude the following. 1) Uniform dosages of nicotine in the rabbit model decreases the vascular ingrowth into autogenous cancellous bone graft. 2) The inhibitory effect of nicotine varies between animals, suggesting predisposition in some. 3) The vascular effects are reversible within 2 weeks of elimination of nicotine, although late bony resorption continues beyond the time of high serum nicotine levels.

Sternal release and advancement with thoracotomy and osteotomy for idiopathic osteopenia.

Transient neurologic changes developed in a rare case of progressive thoracic kyphosis secondary to idiopathic osteopenia with marked spinal and chest cage deformities. The patient underwent correction by both anterior thoracic and posterior spinal approaches, with concomitant sternal release and advancement. After 16 months he continues to have good anatomic and functional results.

The effect of nicotine on spinal fusion.

STUDY DESIGN: An animal model of posterior lateral intertransverse process fusion healing in the face of systemic nicotine. OBJECTIVES: To evaluate the effect of systemic nicotine on the success of spinal fusion and its effect on the biomechanic properties of a healing spinal fusion in an animal model. SUMMARY OF BACKGROUND DATA: Clinical observations suggested that cigarette smoking interferes with the healing of bony fusion. No direct link has been made to implicate nicotine as a cause for impaired healing of spinal fusions or fractures. METHODS: Twenty-eight adult female New Zealand white rabbits underwent single level lumbar posterior lateral intertransverse process fusion using autologous iliac bone graft. Animals were randomly assigned to either receive systemic nicotine or receive no nicotine. Animals were killed 35 days after surgery. Manual testing of the fusion mass was performed to determine the fusion status. Each fusion mass underwent biomechanic testing. RESULTS: Fifty-six percent of the control animals were judged to have solidly fused lumbar spines, and there were no solid fusions in the nicotine group (P = 0.02). The mean relative fusion strength in the control group was greater (P = 0.09) than in the nicotine group. For the comparable stiffness figures, the control group was greater than the nicotine group (P = 0.08). CONCLUSIONS: This animal model established a direct relationship between the development of a nonunion in the presence of systemic nicotine. The results suggested that bone formed in the face of systemic nicotine may have inferior biomechanic properties.

Compartment pressure in association with closed tibial fractures. The relationship between tissue pressure, compartment, and the distance from the site of the fracture.

We studied twenty-five consecutive patients who had a closed tibial fracture to determine whether there was a relationship between compartment pressure and the distance at which the pressure was measured from the site of the fracture. Tissue pressure was measured in all four compartments of the leg at the level of the fracture and at five-centimeter increments proximal and distal to the fracture. The peak pressure was usually found at the level of the fracture and was always located within five centimeters of the fracture. The highest pressures were recorded in the anterior and the deep posterior compartments in twenty patients, including all five of those who had had a fasciotomy. The measured pressure decreased steadily when sampled at increasing distances proximal and distal to the site of the highest recorded pressure. Decreases of twenty millimeters of mercury (2.67 kilopascals) five centimeters adjacent to the site of the peak pressure were common. Compartment syndrome was diagnosed in five patients on the basis of clinical findings, and the diagnosis was confirmed when peak compartment pressures of more than the critical threshold (within twenty millimeters of mercury [2.67 kilopascals] of the diastolic blood pressure) were recorded. Three of these five patients had measured pressures that were less than the critical threshold within five centimeters of the site of the peak pressure. Failure to measure tissue pressure within a few centimeters of the zone of peak pressure may result in a serious underestimation of the maximum compartment pressure. Our results suggest that measurements should be performed in both the anterior and the deep posterior compartments at the level of the fracture as well as at locations proximal and distal to the zone of the fracture to determine reliably the location of the highest tissue pressure in a lower extremity when a compartment syndrome is suspected clinically. The highest pressure should be used in the decision-making process.

Determination of the compartment pressure threshold of muscle ischemia in a canine model.

A canine model was used to test the hypothesis that critical intracompartmental pressure leading to ischemic muscle necrosis is linked to diastolic blood pressure. Twenty adult dogs were subjected to an infusion of autologous plasma into the anterolateral muscle compartment of the left hindlimb to create an elevation in compartment pressure. There were four experimental groups of five dogs each. In group I, the compartment pressure (CP) was maintained at the animals' diastolic blood pressure (DBP); in group II, at 10 mm Hg less than the DBP; in group III, at 20 mm Hg less than the DBP; and in group IV, at 30 mm Hg. The pressure was measured continuously in the proximal, central, and distal segments of the compartment during an 8-hour period. Immediately postoperatively, and, on the first, fourth, seventh, and fourteenth days one animal from each group was killed. The tibialis cranialis muscle was then removed and analyzed using light and electron microscopy. The critical pressure threshold for ischemic muscle necrosis was found to be 20 mm Hg less than the diastolic blood pressure.

Nicotine on the revascularization of bone graft. An experimental study in rabbits.

STUDY DESIGN: In 24 rabbits, the authors transplanted autologous cancellous bone to the anterior chamber of the eye. Half of the rabbits received nicotine and half received placebo (albumin) from mini-osmotic pumps that were implanted subcutaneously. Revascularization of the bone graft was evaluated postoperatively using ophthalmology slit-lamp and fluorescein angiography, and after sacrifice using microvascular silicone injection and histology. OBJECTIVES: The hypothesis that nicotine inhibits the revascularization of bone graft because of its pharmacologic action on the microvasculature was tested. SUMMARY OF BACKGROUND DATA: Pseudoarthrosis after spinal fusion occurs more frequently in smokers as compared with nonsmokers. METHODS: Observations of the bone graft were made regarding the time after implantation when vessels within the graft were noted and the pattern of these vessels. Revascularization of the graft was graded based on the observed percent area of fluorescence after injection of fluorescein. Serum levels of nicotine were measured weekly. Colored silicone was injected at sacrifice to fix the vasculature of the bone graft. Histologic analysis of undecalcified sections was performed. RESULTS: Nicotine, as compared with placebo, was associated with delayed revascularization within the graft, a smaller percent area of revascularization, and a larger number of grafts showing necrosis. CONCLUSIONS: Nicotine inhibits, but does not prevent, the revascularization of cancellous bone grafts. Inhibition of early revascularization by nicotine is proposed as the pathophysiologic mechanism by which smoking may adversely affect the healing of spinal fusions.

Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model.

Our objective was to define the critical tissue pressure at which irreversible muscle damage occurs and to compare our results to those thresholds advocated in the orthopaedic literature. A standard plasma infusion compartment syndrome model was created in a canine model. Four dogs were in each of four experimental groups with compartment pressure maintained as follows: (a) 30 mm Hg with support of diastolic blood pressure to a level > 50 mm Hg; (b) 20 mm Hg less than diastolic pressure; (c) 10 mm Hg less than diastolic blood pressure; (d) a level equal to the animal's diastolic blood pressure. All animals were sacrificed 14 days after the procedure. Histology revealed the following: (a) tissues pressurized to 30 mm Hg in a normotensive dog demonstrated no significant abnormalities; (b) tissues pressurized to 20 mm Hg less than diastolic revealed occasional cells undergoing regeneration but no evidence of infarction or fibrosis; (c) tissues pressurized to 10 mm Hg less than diastolic showed scattered small areas of infarction and fibrosis; and (d) tissues pressurized to diastolic blood pressure demonstrated more widespread infarction and scarring. The ischemic threshold of muscle, beyond which irreversible tissue damage occurs, is directly related to the difference in compartment and perfusion pressure. Our findings document this pressure to be 10 mm Hg less than diastolic blood pressure or within 30 mm Hg of mean arterial pressure. This data refutes the use of absolute tissue pressure values as a guide to the necessity of fasciotomy. To abort an impending compartment syndrome and avoid irreversible tissue injury and their sequelae, fasciotomy should be done if tissue pressure reaches within 10-20 mm Hg of diastolic pressure.

Intracompartmental pressure measurements in the normal forearm.

In 20 normal subjects, intracompartmental pressure measurements were made at three different sites in the volar forearm: half the distance between the medial epicondyle and ulnar styloid and at points 4 cm proximal and 4 cm distal. The pressure measurements were made using a hand-held digital compartment pressure monitor. The study demonstrated that in the uninjured volar compartment, clinically significant (5 mm Hg) intracompartmental pressure differences exist over distances as little as 4 cm.

The force exerted by the halo pin. A study comparing different halo systems.

Seven different halo systems were evaluated biomechanically to compare the force exerted by the halo pin in each system. In three different experiments torque values of 2, 4, 6, 7, and 8 in lb were applied to the halo pin, and the force at the skull end of the halo pin was measured using a load cell. In the first experiment, the threads on the halo pin were dry, in the second experiment saline was applied to the threads on the pin, and in the third experiment cadaveric bone from the skull was interposed between the pin and the load cell. The results showed that for a given value of applied torque to the pin, the force exerted by the pin end varied widely according to the halo system and whether or not the pin was "lubricated."

Surgical reconstruction of late post-traumatic thoracolumbar kyphosis.

Thirty-four patients underwent surgery for late post-traumatic thoracolumbar kyphosis. Indications for surgery included increasing kyphotic deformity, pain, or increasing neurologic deficit. Procedures included anterior spinal fusion only, posterior spinal fusion only, anterior and posterior fusions as staged procedures, and anterior and posterior fusions under the same anesthetic. Eighteen of the patients with anterior fusions also underwent decompression of the spinal cord by resection of the vertebral body. Stable fusion with halt in progression of deformity was obtained in 33 of the 34 patients by following basic biomechanical principles.