Anulus Fibrosus

The anulus fibrosus is a laminate structure surrounding the central nucleus pulposus and inserting into the endplates and the vertebral body. It consists primarily of water, collagen, proteoglycans, and noncollagenous proteins. The laminates are organized in layers mainly composed of type I collagen fibers, which alternate in angles with respect to the transverse plane. Between the layers are so-called interlaminar spaces containing proteoglycans (aggrecan, versican) and other linking elements.⁴ In the center, the fibers insert into the cartilaginous endplates, and in the periphery they bypass the endplates and insert into the bone, called Sharpey fibers. The inner and outer parts of the anulus differ in that in the inner part the layers are less well organized and more widely spaced. The proportion of type I collagen increases from the inner anulus to the outer anulus, whereas type II collagen is more common in the inner anulus than outer anulus. Small proteoglycans (decorin and biglycan) are found primarily in the outer anulus, whereas elastin is present throughout. Elastin constitutes 1.7% to 2% of the dry weight of the anulus. In the outer anulus, elastin is present within the lamella running parallel to the collagen and in the same direction.^5,24 In the inner anulus, elastin is also organized within the lamellae. Fiber networks bind adjacent lamella together preventing them from separating.^6,7 Table 47–1 compares the outer anulus and inner anulus.

TABLE 47–1 Comparison of the Outer Anulus and Inner Anulus

The cell density in the anulus pulposus is about twice the cell density of the nucleus pulposus.⁸ In the outer anulus, the cells are fusiform-shaped and align with the collagen fibers alternating with each lamella. These cells produce mainly type I collagen. In the inner anulus, the cells are more similar to the cells of the nucleus pulposus. They are chrondrocyte-like and produce mainly type II collagen.

The mechanical exposure of the different parts of the anulus is initially different. The inner anulus is primarily subjected to the hydrostatic pressures of the nucleus pulposus, whereas the outer anulus is more under compression or tension depending on the direction of movement. Similar to other connective tissue structures, the anulus is anisotropic and adapted to the principal directions of load.

Effect of Aging on Anulus Fibrosus

Various chemical and structural changes occur with aging. These changes seem to occur first in the inner anulus, which loses a large part of its proteoglycan and water and gradually assumes a more nucleuslike structure.² The overall proteoglycan and collagen concentrations decrease with aging, probably reflecting a decrease in cellular biochemical activity. Among smaller nonaggregating proteoglycans, decorin levels decrease with aging in the outer anulus, and biglycan and fibromodulin levels increase. In the inner anulus, decorin levels have been found to increase with aging.

Healing of Anulus

Early studies in dogs showed comparatively poor healing when larger defects were created in the annular wall.⁹ Smith and Walmsley¹⁰ reported that after an incision the outer anulus healed by fibrous tissue ingrowth from the sides and that there was also a gradual healing of the inner anulus over a 1-year period. Long-term collagen fibers gradually invaded the nuclear tissue, of which some remained in the annular incisions. Fazzalari and colleagues,¹¹ using an ovine model, introduced needle punctures and concentric tears and tested the specimen mechanically up to 18 months. Significant changes occurred in disc biomechanics in both cases and remained significant over time. The annular lamellae thickened, and the adjacent vertebral body bone volume fraction increased. Although this model is not a herniation model, it shows the poor healing of concentric tears and their effect on the disc biomechanics. There is limited information on annular repair in humans after discectomy. Current information suggests a limited healing potential after annulotomy. This increases the risk of reherniation. Reoperation rates for recurrent herniations ranging from 3% to 27% have been reported.^12–15 The frequency of reoperations seems to be related to the size of the annular defect.

Biologic Repair

At least four types of annular repair are discussed in the literature: collagen modification, cell therapy, gene therapy, and tissue engineered scaffolds. Gene and cell therapies are unlikely to repair existing cracks, tears, and incisions unless combined with scaffolds. Numerous studies have been published in which scaffolds have been populated with cells, and various success rates have been reported. Most of these studies have been performed in vitro, but a few animal studies have been reported. Gene and growth factor therapies can repair annular needle punctures in the early stages. Many growth factors seem to have a stronger effect on proteoglycan than collagen. Zhang and colleagues¹⁶ reported that collagen synthesis was enhanced by BMP-13 and Sox9.

Bron and colleagues³ listed requirements for anulus fibrosus scaffolds. The scaffolds should: