Post-Operative Bone Growth Stimulant Introduction Method

Abstract

A method of revising a patient having a fusion cage implanted within a spinal column, involving percutaneously delivering a first end of a tube to the spinal column, fluidly connecting the first end of the tube to the fusion cage, and delivering a bone growth agent into the fusion cage through the tube.

Description

CONTINUING DATA[0001]This patent application is a continuation of and claims priority from co-pending U.S. Ser. No. 14 / 481,827, filed Sep. 9, 2014, entitled “Post-Operative Bone Growth Stimulant Introduction Method”, Jacobs et al., (Docket No. DSP5062USNP), which claims priority from U.S. provisional patent application Ser. No. 61 / 947,642, filed Mar. 4, 2014, entitled “Post-Operative Bone Growth Stimulant Introduction Method”, Jacobs et al., (Docket No. DSP5062USPSP), the specifications of which are incorporated by reference in their entireties.BACKGROUND OF THE INVENTION[0002]The natural intervertebral disc contains a jelly-like nucleus pulposus surrounded by a fibrous annulus fibrosus. Under an axial load, the nucleus pulposus compresses and radially transfers that load to the annulus fibrosus. The laminated nature of the annulus fibrosus provides it with a high tensile strength and so allows it to expand radially in response to this transferred load.[0003]In a healthy interverteb...

AI Technical Summary

Benefits of technology

[0013]The present invention relates to a novel method of revision that delivers a bone growth agent to the implanted cage. Preferably, a tube is percutaneously delivered to the cage site and docked to the cage, any tissue that has grown into the cage is removed through the tube, and bone growth agent is then delivered through the tube to the cage. This method eliminates the need for cage removal, thereby reducing the risk and cost associated with the revision.Therefore, in accordance with the present invention, there is provided a method of revising a patient having a fusion device having a cavity implanted within a spinal column, comprising the steps of:

Problems solved by technology

In other instances of DDD, genetic factors or apoptosis can also cause the cells within the nucleus pulposus to emit toxic amounts of these cytokines and MMPs.

In some instances, the pumping action of the disc may malfunction (due to, for example, a decrease in the proteoglycan concentration within the nucleus pulposus), thereby retarding the flow of nutrients into the disc as well as the flow of waste products out of the disc.

This reduced capacity to eliminate waste may result in the accumulation of high levels of toxins that may cause nerve irritation and pain.

As DDD progresses, toxic levels of the cytokines and MMPs present in the nucleus pulposus begin to degrade the extracellular matrix, in particular, the MMPs (as mediated by the cytokines) begin cleaving the water-retaining portions of the proteoglycans, thereby reducing its water-retaining capabilities.

This degradation leads to a less flexible nucleus pulposus, and so changes the loading pattern within the disc, thereby possibly causing delamination of the annulus fibrosus.

These changes cause more mechanical instability, thereby causing the cells to emit even more cytokines, thereby upregulating MMPs.

As this destructive cascade continues and DDD further progresses, the disc begins to bulge (“a herniated disc”), and then ultimately ruptures, causing the nucleus pulposus to contact the spinal cord and produce pain.

These revisions are expensive and pose significant safety risks to the patient.

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