WO2007059328A2

WO2007059328A2 - Selective molecular transport through modified disc shunt

Info

Publication number: WO2007059328A2
Application number: PCT/US2006/044795
Authority: WO
Inventors: James E. Kemler; Jeffrey E. Yeung
Original assignee: Kemler James E; Yeung Jeffrey E
Priority date: 2005-11-19
Filing date: 2006-11-17
Publication date: 2007-05-24
Also published as: WO2007059328A3

Abstract

The disc contains no blood vessels. Nutrients and oxygen essential to disc cells are diffused from adjacent vertebral bodies into the disc. As we age, calcified layers form between the disc and vertebral bodies, blocking diffusion. The disc begins to starve and flatten. The weight shifts abnormally from disc to the facet joints causing strain and pain. Hydrophilic or charged groups are proposed bonding to disc shunts to facilitate the exchange between the avascular disc and bodily circulation. In addition, bonding of cleavable hydrophobic groups delays or hinders transport to minimize infiltration of immunoglobulins or cytokines into the immuno-isolated disc.

Description

SELECTIVE MOLECULAR TRANSPORT THROUGH MODIFIED DISC SHUNT

James E. Kemler, Jeffrey E. Yeung

FIELD OF INVENTION

The disc shunt is used to re-establish the exchange of nutrients and waste between the avascular disc and bodily circulation to alleviate back pain. This invention relates to chemical or physical modification of the disc shunt for enhancing, selecting or -delaying molecular transport into and out of the avascular disc.

BACKGROUND

Low back pain is a leading cause of disability and lost productivity. Up to 90% of adults experience back pain at some time during their lives. For frequency of physician visits, back pain is second only to upper respiratory infections. In the United States, this malady disables 5.2 million people, and the economic impact has been reported to be as high as $100 billion each year. Though the sources of low back pain are varied, in most cases the intervertebral disc is thought to play-a-central role. Degeneration of .the disc initiates pain in other tissues by altering spinal mechanics and producing non-physiologic stress in surrounding tissues.

The intervertebral disc absorbs most of the compressive load of the spine, but the facet joints of the vertebral bodies share approximately 16%. The disc consists of three distinct parts: the nucleus pulposus, the annular layers and the cartilaginous endplates. The disc maintains its structural properties largely through its ability io attract-and retain water. A normal disc contains 80% water in the nucleus pulposus. The nucleus pulposus within a normal disc is rich in water absorbing .sulfated -glycosaminogly cans (chondroitin and keratan sulfate), creating the swelling pressure to provide tensile stress within the collagen fibers of the annulus. The swelling pressure produced by Jiigh water -content is crucial to supporting the annular layers for sustaining compressive loads. In adults, the intervertebral disc is avascular. .Survival of the disc .cells depends on diffusion of nutrients from external blood vessels and capillaries through the cartilage of the endplates. Diffusion of nutrients also permeates from peripheral blood vessels adjacent to the outer annulus, but these nutrients can only permeate .up to 1 cm^jnto the annular layers of the disc. An adult disc can be as large as 5 cm in diameter; hence diffusion through the cranial and caudal endplates is crucial for maintaining the health of the nucleus pulposus and inner annular layers of the disc.

Calcium pyrophosphate and hydroxyapatite-are commonly found in -the endplate and nucleus pulposus. Beginning as young as 18 years of age, calcified layers begin to accumulate in the cartilaginous endplate. The blood vessels and capillaries at the -bone- cartilage interface are gradually occluded by the build-up of the calcified layers, which form into bone. Bone formation at the endplate increases with age.

When the endplate is obliterated by bone, diffusion of nutrients through the calcified endplate is greatly limited. In addition to -hindering the diffusion of nutrients, xalcifϊed endplates further limit the permeation of oxygen into the disc. Oxygen concentration at the central part of the nucleus is extremely low, -Cellularity of the -disc is already low compared to most tissues. To obtain necessary nutrients and oxygen, cell activity is restricted to being on or in very close proximityJ;o the cartilaginous-endplate. Furthermore, oxygen concentrations are very sensitive to changes in cell density or consumption rate per cell.

The supply of sulfate into the nucleus pulposus for biosynthesizing sulfated glycosaminoglycans is also -restricted by the calcified endplates. As a result, ihe sulfated glycosaminoglycan concentration decreases, leading to lower water content and swelling pressure within the nucleus pulposus. During normal daily compressive loading-on the spine, the reduced pressure within the nucleus pulposus can no longer distribute forces evenly along the circumference of the inner annulus to keep the lamellae bulging outward. As a result, the inner lamellae sag inward, while the outer annulus continues to bulge outward, causing delamination of the annular layers.

The shear stresses causing annular delamination and bulging are highest at the posteriolateral portions adjacent to the neuroforamen. The nerve is confined within -the neuroforamen between the disc and the facet joint. Hence, the nerve at the neuroforamen is vulnerable to impingement by the bulging disc or bone spurs. When oxygen concentration in the disc falls below 0.25 kPa (1.9 mm Hg), production of lactic acid dramatically increases with increasing distance from the.endplate. The pH within the disc falls as lactic acid concentration increases. Lactic acid diffuses through micro-tears of annulus irritating the richly innervated posterior longitudinal ligament, facet joint and/or nerve root. Studies indicate that lumbar pain correlates well with high lactate levels and low pH. The mean pH of symptomatic discs was significantly lower than the mean pH of normal discs. Acid concentration is three times higher in symptomatic discs than normal discs. In symptomatic discs with pH 6.65, the acid concentration within the disc is 5.6 times the plasma level. In some preoperative symptomatic discs, nerve roots were found to .be surrounded by dense fibrous-scars and adhesions with remarkably lowpH 5.7-6.30. The acid concentration within these discs was 50 times the plasma level.

Approximately 85% of patients with low back pain cannot be given a precise pathoanatomical -diagnosis. This type of pain is generally classified under "non-specific pain". Back pain and sciatica can be recapitulated by maneuvers that do not affect the nerve root, such as intradiscal saline mjection,-discography,^nd^ompression-of the posterior longitudinal ligaments. It is possible that some of the non-specific pain is caused by lactic acid irritation secreted from the disc. Injection into .the disc .can flush out the lactic acid. Maneuvering and compression can also drive out the irritating acid to produce non-specific pain. Currently, no intervention other -than -diskectomy .can-halt the production of lactic acid.

In the presence of oxygen, metabolism ofeach glucose-molecule produces 36 adenosine triphosphates, ATP, through glycolysis, citric acid cycle and electron transport chain. ATP is a high energy compound -essential for driving .biosynthesis of the-water- retaining proteoglycans. Under anaerobic conditions, the metabolism ofeach glucose molecule produces only 2 ATP and two lacticacids. Hence, production of high-energy compound ATP is low under anaerobic conditions within the disc.

The nucleus pulposus is thought to function-as "the air in.a tire" to pressurize the disc. To support the load, the pressure effectively distributes the forces evenly along the circumference of the inner annulus and keeps the lamellae bulging outward. The process of disc degeneration begins with calcification of the endplates, which hinders diffusion of sulfate and oxygen into the nucleus pulposus. As a result, production of the water absorbing sulfated glycosaminoglycans is significantly reduced, and the water content within the nucleus decreases. The inner annular lamellae begin to sag inward, and the tension on collagen fibers within the annulus is lost. The degenerated disc exhibits unstable movement, similar to a flat tire. Approximately 20-30% of low-back-pain patients have been diagnosed as having spinal .segmental instability. The pain may originate from stress and increased load on the facet joints and/or surrounding ligaments. In addition, pH within the disc becomes acidic -from the anaerobic production~of lactic acid, which irritates adjacent nerves and tissues. Shunts or conduits for re-establishing the exchange of nutrients and waste between the degenerative disc and bodily circulation is described in PCT/US2004/14368 (WO 2004/101015) and US applications 10/840,816 by J. Yeung-and T. Yeung, both applications filed on May 7, 2004. US provisional patent application 60/626644, filed on November 10,,2004 by Jeffrey E. Yeung also described several disc shunt (conduit) configurations and delivery devices.

Discs L4-5 and L5-S1 are shielded by the iliac, inaccessible by straight needle from outside to deliver the conduit into the disc. However, through the pedicle of the vertebral body, the elastically curved needle proposed in PCT/US2005/22749, filed on June 22, 2005 by J. Yeung, can puncture through the calcified endplate to deliver the shunt or conduit for exchanging nutrients and lactate between the avascular disc and bodily circulation.

The disc shunt is designed to transport lowumolecular weight nutrients, waste and gaseous molecules. Many nutrients contain positive charges in physiological pH, including glucosamine, galactosamine, lysine,-arginine, histidine and others. Many other nutrients contain negative charges in physiological pH, including sulfate, glucuronate, galacturonate, aspartate, glutamate and others. Primary waste within the disc is the negatively charged lactate, pKa = 3.79 at 25⁰C. By modifying the disc shunt with ionic elements, through charge-charge or affinity interaction, transport of nutrients and waste may be selected or enhanced to reverse disc regeneration. By re-supplying the disc cells with nutrients, biosynthesis of sulfated glycosaminoglycans may increase to retain additional water and sustain compressive loading. Hence, segmental instability and excessive loading of facet joints are minimized to alleviate back pain. With the presence of additional oxygen, production of lactic acid may decrease to minimize acidic irritation and increase production of ATP, driving biosynthesis of the water-retaining proteoglycans. SUMMARY OF INVENTION

The disc shunt is chemically or physically modified to enhance, .select or delay molecular transport into and out of the avascular disc. Most vital nutrients in serum are water soluble. Hydrophilic modification on the-disc shuntcan enhance the rate of transport of water soluble nutrients into the avascular disc. Galactosamine, glucosamine and glucuronic acid are repeating -disaccharideJπiilding blocks of the water-retaining chondroitin sulfate, keratan sulfate and hyaluronic acid. In physiological pH, galactosamine, glucosamine-and glucuronic acid in serum contain net charges. Linking charge groups on the disc shunt may further increase affinity to capture, or accumulate these nutrients through charge-charge attractioii-andlransport into thexlisc. To further minimize the potential of immunoglobulin infiltration through the shunt into the immuno-isolated disc, the disc shunt is .bonded with-cleavable hydrophobic molecules. After formation of fibrous encapsulation over the shunt, the cleavable molecules hydrolyze to shed the hydrophobic portion, becoming hydrophiliαgroups bonded to the fibrous encapsulated shunt. The immunoglobulins are too large to penetrate through the fibrous tissue, while the^small nutrients readily-diffuscand-infiltrate through the shunt into the avascular disc.

REFERENCE NUMBER

100 Intervertebral disc

101 Needle or sheath 105 Endplate

106 Hyaline cartilage

107 Capillaries

108 Calcified layer or blockade

109 Plunger 112 Blood vessels 121 Neuroforamen 123 Spinal cord

126 Conduit or shunt

128 Nucleus pulposus

129 Facetjoint 142 Superior articular process

143 Inferior articular process

144 Blunt rod

159 Vertebral body 194 Nerve root 195 Posterior longitudinal ligament 220 Rigid needle 230 Dilator 278 Pedicle

359 Filament t>r matrix of disc shunt DESCRIPTION OF THE DRAWINGS

Figure 1 depicts a superior view of -the vertebral body 159 with,the rigid needle-220 puncturing through the pedicle 278.

Figure 2 shows insertion of the rigid needle-220 containing plastically -curv-ed-needle or sheath 101, shunt 126 and plunger 109 through the pedicle 278 of the vertebral body 159.

Figure 3 shows deployment of the elastically curved needle 101 from the rigid needle 220, puncturing through-thexalcified-endplateJL05 into the intervertebral -disc J.00.

Figure 4 shows retrieval of the elastically curved needle 101 into the rigid needle 220, The plunger 109 ias been held stationary Jo deploy the shunt 126 bridging the^ertebral body 159 to the disc 100.

Figure 5 shows a superior view of an endplate 105 punctured by. the-elastically .curved needle 101 carrying the shunt 126 into disc space.

Figure 6 shows the top view of the endplate-shunt 126-afterj-etrievaLof the elastically curved needle 101 into the rigid needle 220. Figure 7 shows an anterior approach of a needle or sheath 101, shunt 126 and plunger 109 puncturing through the endplate 105 intoihe-disc 100 to-deliver an endplate shunt 126.

Figure 8 shows the endplate shunt 126 bridging between the vertebral body 159 and the disc 100.

Figure 9 depicts insertion of the needle 101,-shunt 126, plunger 109 andsleeve.220 assembly into a dilator 230 leading into the disc 100.

Figure 10 shows deployment of the curved-needle lOlJhrough-the.calcified-endplate 105. Figure 11 depicts withdrawal of the needle 101 while the plunger 109 is held stationary to dislodge the shunt 126 through the calcified endplate 105.

Figure 12 shows deployment x>f two- shuntsJL26 through-superior_and inferior .calcified endplates 105.

Figure 13 indicates-disc 100-height restoration from .regained swelling pressure within the nucleus pulposus 128 due to re-establishment of nutrient and waste exchange.

Figure 14 depicts two shunts 126 providing-nutrient.and waste.exchange to -the nucleus pulposus 128 of a regenerated disc 100.

Figure 15 depicts a longitudinal view of a-shunt 126 being delivered transversely across a degenerated disc 100. Figure 16 shows protrusion of the -annular shunt 126 from the -degenerating .disc 100 to re-establish the exchange of nutrient and waste between disc 100 and surrounding serum.

Figure 17 depicts a regenerated disc 100 with exchange of nutrients and waste through the annular shunt 126. Figure 18 shows a methanol radical as a reactant to the disc shunt 126.

Figure 19 shows linkages of hydroxyl groups (-OH) onthematrix-orfilarnents359-of a disc shunt 126 to provide the hydrophilic property and hydrogen bonding with sugars.

Figure 20 shows a radical aceticacid-as-a reactant to thexlisc shunt 126.

Figure 21 shows linkages of carboxyl groups (-COO^") forming anionic charges on the matrix or filaments 359 to attract the positively charged nutrients.

Figure 22 shows a radical methylamine as a reactant to disc shunt 126. Figure 23 shows linkages of amines groups (-NHs⁺) forming cationic groups on the matrix or filaments .359 -to-attract sulfate,-aspartate-and-glutamate.

Figure 24 shows a radical isobutane as a hydrophobic reactant to disc shunt 126.

Figure 25 shows linkages of isobutanes forming hydrophobic .groups on thejnatrix 359 of a disc shunt 126 to minimize potential infiltration of immunoglobulins into the immuno-isolated disc.

Figure 26 shows multiple modifications on the matrix or filaments 359 to capture various substrates and control infiltration through the disc shunt 126.

Figure 27 shows hydration of an ester bond converting the hydrophobic property of a disc shunt 126io a hydrophilic property with~a negative charge.

Figure 28 shows hydration of an activated amide bond converting the hydrophobic property of a disc shunt 126 to a. hydrophilic property with-a positivexharge.

Figure 29 shows hydration of a thiol ester bond after fibrous encapsulation, converting the hydrophobic -property Ofa-disc-shunt 126 to-a hydrophilic property. DETAILED DESCRIPTION OF THE EMBODIMENTS

The disc shunt 126 -can be implanted througha-minimally invasive procedure Jhrough the pedicle 278 and calcified endplate 105 into the degenerated disc 100, as shown in Figures 1 -6. The pedicle .278 approach is particularly useful for the Jower lumbar discs, L4-5, L5-S1, which are shielded by a pair of ilia. The disc shunt 126-jcan also be implanted to prevent progressive-degeneration of the discs adjacent 100 to spinal fusion or disc replacement. Figures 7-8 show implantation of an endplate shunt 126 through the vertebral body 159 into ihe 4isc 100.adjacent io-a level receiving spinal fusion or disc replacement through anterior approach.

The needle 101 can_also directly deliver Ihe-disc shunt 126 into-a-disc 100_aboveihe ilium, such as the L3-4, as shown in Figures 9-11. The endplate shunts 126 traverse the calcified endplates JL05 to re-establish the jexchange of nutrients and-waste .between the degenerating disc 100 and vertebral body 159, as shown in Figure 12.

In the presence of oxygen delivered .throughihe shunt.126, biosynthesis ofJacticacid is minimized, hi addition, the lactic acid can escape during compressive loading of the degenerated disc 100 -through the shunt 126. As-a ϊesuhVacidic irritation is minimized. Furthermore, under anaerobic conditions, metabolism of each glucose molecule produces only 2 ATP and two lactic acids. In-aerobic condition, glycolysis, .citric acid cycle and electron transport chain produce 36 adenosine triphosphates. ATP, from each glucose molecule. ATP is the high energy compound essential for driving biochemical reactions, including the biosynthesis of the water retaining proteoglycans for sustaining compressive loads on the disc 100.

A continual supply of nutrients and oxygen enhances production of proteoglycans to retain additional water and re-pressurize the disc 100, as-shown in Figures 13 -AA. As a result, the compressive load is shifted from the strained facet joints back on to the regenerated disc 100 to alleviate back pain.

The exchange of nutrients and waste between the degenerated disc 100 and the peripheral fluid surrounding the disc 100 canalso be provided by an.annular shunt 126 protruded from the disc 100, as shown in Figures 15-17.

Increasing the hydrophilic property of thejshunt 126 can-enhance the rate of nutrient and waste exchange. Plasma treatment using oxygen can provide the hydrophilic hydroxyl group, - OH, onihe polymeric discshunt 126. The hydroxy! groups form the hydrogen bonds with water molecules to increase hydrophilic property and capillarity of the disc shunt 126.

Figure 18 shows a methanol radical, which can be generated by plasma or chemical to form hydroxyl groups (- OH) on ihe -filaments 359 of the .shunt 126, as .shownin Figure 19. The hydroxyl groups increase binding affinity by hydrogen bonding to glucose, galactose, glucosamine,-andgalactosarnine from serum to-enhance transport through the shunt 126 into the disc 100 for biosynthesizing the water-retaining proteoglycans. The hydroxyl groups of the disc shunt 126-also-enhance transport of hydrophilic nutrients, including most amino acids essential to build proteoglycans and collagen.

In general, the hydroxyl or hydrophilic groups alter the water contact angle on the matrix or filaments 359 to enhance capillary action of the disc shunt 126. As a result, rate of exchange between the disc 100 and bodily circulation increases.

Figure 20 shows a molecular structure of acetate radical, which can be generated by plasma or chemical to form carboxyl group (- COO^") on the filament 359 with a negative charge, as shown in Figure 21. Similarly, formic acid (HCOOH) can also be used to generate the carboxyl group. The negative charge creates a strong affinity to select and transport positively charged glucosamine and galactosamine. Glucosamine is a building block of keratan sulfate and hyaluronic acid; galactosamine is a building block of chondroitin sulfate. Both are nutrients crucial for biosynthesizing proteoglycans. Figure 22 shows a molecular structure of methyl amine radical, which can be generated by plasma or chemical to form a primary amine (- NH₃ ⁺) with a positive charge on the shunt 126, as shown in Figure 23. Ammonia (NH₃) can also be used to form primary amine on disc shunt 126. The positively charged shunt 126 creates a strong affinity to sulfate (- SO₄ ^"2), glucuronic acid, lactic acid and two carboxylic amino acids in neutral pH. Sulfate is-a crucial ingredient for biosynthesizing chondroitin-sulfate and keratan sulfate. Glucuronic acid is one of the repeating disaccharide of chondroitin sulfate and hyaluronic acid, the backbone .of water-retaining proteoglycans within the avascular disc 100. Lactic acid is an irritant and waste from the avascular disc 100. Amino acids are essential for biosynthesizing-prαteoglycans-and collagen. Jn_essence,ihe positively charged shunt 126 can enhance the exchange of essential nutrients and irritable waste between the disc 100 and bodily circulation.

To minimize the potential of immunoglobulin infiltration through the shunt 126 into the immuno-isolated disc 100, ihe disc shunt 126 can be bonded with.a hydrophobic molecule, such as the isobutane radical, as shown in Figure 24. The hydrophobic property minimizes infiltration of the large-and-highly water soluble immunoglobulins into the disc shunt 126, as shown in Figure 25. With adequate hydrophobic modification, the large immunoglobulins are repelled from entering in the filament 35ft. On-the other hand, the small nutrients and waste can penetrate between the sparsely linked hydrophobic molecules into the filament359 for-transportingihroughlhe shuntJU26. Disc shunt 126 can be modified with various functional groups, including hydrophilic, hydrophobic, negatively charged and positively xharged-groups,-as.shownJn Figure 26, to capture and hold various nutrients and waste simultaneously for transport through the shunt 126. In-addition, the shunt 126 can be chemically .modifiedsection by section. Hydrophobic groups can be modified on the section external to the disc 100 to minimize potential infiltration of immunoglobulins. The internal section of the-shuntJ.26 can be modified with hydrophilic or charged groups to facilitate exchange of nutrients and waste.

Fibrous encapsulation over the disc shunt 126 is imminent within one to six months. Diffusion of nutrients through the fibrous tissue is evident by surviving cells within fibrous encapsulation of various implants, including sutures, heart pacers and joint replacements. In addition, the fibrous tissue may serve as a barrier to prevent penetration of the large immunoglobulins or cytokines from reaching the disc shunt 126. The shunt 126 can be chemically modified with cleavable hydrophobic molecules to prevent possible infiltration of immunoglobulins into the disc 100. The ester bonded R group in Figure 27 is hydrophobic to repel immunoglobulins or cytokines from entering the modified shunt 126. After formation of fibrous encapsulation, the ester bond is slowly hydrolyzed to form a carboxylic group bonded to the shunt 126, and a departing alcohol bonded with the hydrophobic group, R. With the carboxyl modification, the fibrous encapsulated shunt 126 becomes hydrophilic with negative charge, facilitating transport of nutrients diffused through the fibrous tissue into the avascular disc 100. Figure 28 shows a shunt 126 modified with a hydrophobic group, R, linked to an electron withdrawing chloro-activated amide bond. After formation of fibrous encapsulation, the activated amide bond is slowly hydrolyzed to form a primary amine bonded to the shunt 126, and a departing carboxyl group bonded with the hydrophobic group, R. With the amine modification, the fibrous encapsulated shunt 126 becomes hydrophilic with positive charge, facilitating transport of nutrients diffused through the fibrous tissue into the avascular disc 100.

Figure 29 shows a shunt 126 modified with a hydrophobic group, R, linked to a thiol ester. After formation of fibrous encapsulation, the thiol ester bond is slowly hydrolyzed to form a sulfhydryl group bonded to the shunt 126, and a departing carboxyl group bonded with the hydrophobic group, R. With the sulfhydryl modification, the fibrous encapsulated shunt 126 becomes hydrophilic, facilitating transport of nutrients diffused through the fibrous tissue into the avascular disc 100. If a regular-ester (- O — CO — ) is used, the hydrophilic hydroxyl group (- OH) will be formed on the filaments 359 of the shunt 126 after departure of the hydrophobic group, R. It is to be understood that the present invention is by no means limited to the particular chemistry and methods disclosed herein and/or shown in the drawings, but also includes any other functional group, activating group, hydrophobic group, hydrophilic group, steric hindrance group, modification, changes or equivalents within the scope of the claims. Many more chemicals, derivatives and reactions for modifying the disc shunt 126 can be used to facilitate the exchange of nutrients and waste and to protect the immuno-isolated disc 100. Any one or more of the chemical or method described may be added to or combined with any of the other chemical or method to create alternate combinations and embodiments. It should be clear to one skilled in the art that the current chemicals, methods, embodiments, materials, constructions, tissues or incision sites are not the only uses for which the invention may be used. Different chemicals, constructions, methods, coating or designs for the modified disc shunt or conduit 126 can be substituted and used. Nothing in the preceding description should be taken to limit the scope of the present invention. The full scope of the invention is to be determined by the appended claims.

MISSING AT THE TIME OF THE

TECHNICAL PREPARATION OF

PUBLICATION

Claims

What is claimed is:

1. A deployment device for deploying a-conduit into an intervertebral disc, the deployment device comprising: a sheath, a conduit sized and configured to fit at least partially within said sheath, said conduit including a charged material,-and a plunger to deploy said conduit.

2. The deployment device Of claim 1, wherehi-said charged material has-a negative charge.

3. The deployment device-of claim 1, wherein.said charged material includesxarboxyl groups.

4. The deployment device of claim 1, wherein said charged material has a positive charge.

5. The deployment device of claim 1, wherein said charged material includes amine groups.

6. The deployment device of claim 1, wherein said charged material is bonded to a based material of said conduit.

7. The deployment device of claim 1 , wherein said charged material is plasma bonded to a base material of said conduit.

8. The deployment device of claim 1, wherein said charged material is chemically bonded to a base material of said conduit.

9. A deployment device for deploying a conduit into an intervertebral disc, the deployment device comprising: a sheath, a conduit sized and configured to fit at least partially within said sheath, said conduit including a hydrophilic material, and a plunger to deploy said conduit.

10. The deployment device of claim 9, wherein said hydrophilic material includes hydroxyl groups.

11. The deployment device-of claim 9, wherein-said hydrophilic material is bonded to a based material of said conduit.

12. The deployment device of claim 9, wherein said hydrophilic .materiaLis plasma bonded to a base material of said conduit.

13. The deployment device of claim 9, wherein-said hydrophilic material is .chemically bonded to a base material of said conduit.

14. A deployment device for deploying a conduit into an intervertebral. disc, the deployment device comprising: a sheath, a conduit sized and configured to fit at least partially within said sheath, said conduit including a-hydrophobic material, and a plunger to deploy said conduit.

15. The deployment device of claim 14, wherein said hydrophobic material isxleavable.

16. The deployment device of claim 14, wherein said hydrophobic material is hydrolizable.

17. The deployment device of claim 14, wherein said hydrophobic material is bonded to a base material of said conduit.

18. The deployment device of claim 17, wherein said hydrophobic material is bonded to said base material only on a selected portion of said conduit.

19. The deployment device of claim 18, wherein said selected portion is configured to be outside the intervertebral -disc once the conduithas been implanted.

20. A deployment device for deploying a conduit into an intervertebral disc, the deployment device comprising: a sheath, a conduit sized and configured to fit at least partially withinjsaid. sheath, said conduit including a negatively charged material, a positively charged material, a hydrophilic material and a hydrophobic material, and a plunger to deploy said conduit.

21. The deployment device of claim -20, wherein ^eacliOf .said materials is concentrated in a selected portion of said conduit.

22. The deployment device of claim 20, wherein any one of said materials is concentrated in a selected portion of said conduit.