Background: Discs are avascular. Oxygen and nutrients are diffused from capillaries in endplates into thick discs. Calcified layers begin to fortify the cartilaginous endplates around age 16, (1) blocking many capillaries, (2) reducing diffusion depths, (3) causing starvation and hypoxia in the mid-disc layer. Starvation triggers enzymatic degradation of proteoglycans in mid-disc layer, leading to desiccation and voids in nucleus, and fissure in annulus. Hypoxia triggers production inflammatory cytokines and lactic acid, leading to pH 5.5-6.5 in mid-disc layer, 5-50X acidity of blood plasma. Lactic acid leaks through the annulus fissure to cause discogenic pain from lactic acid burn, as shown in Figure 1. Conversely, disc matrixes near superior and inferior endplates are in the diffusion zones of bicarbonate (pH buffer), oxygen and nutrients from body circulation, and have neutral pH 7.2.
Proposed Intervention: Percutaneous Disc Scaffold (PDS) is a multi-spiral fluid absorbing filament, a braided nylon #3 suture, for bridging between diffusion zones near superior and inferior endplates to re-establish interstitial fluid exchange between the mid-disc and body circulation. Bicarbonate in blood plasma neutralizes the lactic acid. Oxygen inhibits hypoxic inflammation and is essential to biosynthesize the most water-retaining chondroitin sulfate in proteoglycans. Constant supply of nutrients relieves starvation, Figure 2.
Methods: In-vitro and in-vivo studies are used to verify the intended use, safety and efficacy of the PDS. (1) Fluid transport through the #3 braided nylon suture is verified by capillary action of drawing pork blood. (2) Lactic acid neutralization is verified by titration with fresh pork blood. (3) Safety is verified in sheep discs by histology on tissue response at euthanized time point 1, 3, 12 and 30 months. (4) Efficacy is verified in a pilot clinical study after confirming discogenic pain. PDS is implanted through the discography needle. Visual Analog Pain Score (VAS) and Oswestry Disability Index (ODI) are used to evaluate therapeutic efficacy of PDS at 1-week, 3-, 12- and 24-months.
Results: (1) Fluid transport through the #3 braided nylon suture as PDS is demonstrated by capillary action of drawing pork blood 10.3 +/- 1.2 cm against gravity. (2) Approximately 0.51-1.51 cc of pork blood is required to neutralize 1 cc of 2-6 mM lactic-acid, common concentration in painful disc. (3) PDS is inert, elicited no immune response in sheep discs euthanized at 1, 3, 12 and 30-months. (4) Baseline or pre-PDS VAS was 6.1±1.6, and 2-Year VAS after PDS is 1.2±0.7. Baseline ODI was 37.9±15.1%, and 2-Year ODI is 9.8±5.1%.
Conclusion: Acid-base neutralization is instantaneous, which may be the reason for rapid reduction of discogenic pain from lactic acid burn.