CHAPTER 47 Annular Repair
The anulus fibrosus is an important part of the intervertebral disc. Similar to the other disc components, the anulus undergoes changes with aging and with degeneration.1,2 The degenerative process leads to a weakening of the anulus, and delamination, fissures, and cracks occur. Occasionally, the nucleus pulposus can herniate into the cracks and through the entire annular wall. Also, as part of surgical procedures to address contained disc herniations, iatrogenic holes in various shapes and locations are made into the anulus.
In recent years, there has been increasing interest in strengthening the annular structure, which is important to regain the normal function of the disc.3 There is also interest in repairing degenerative and iatrogenic cracks, tears, and holes in the anulus to prevent recurrence of disc herniations and to slow the degenerative process after discectomy. This chapter reviews some of these strategies and puts them in the context of successful treatment of different types of painful spinal conditions. The focus is on the lumbar discs.
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.
| Outer Anulus | Inner Anulus | |
|---|---|---|
| Collagen | 40%-60% dw | 25%-40% dw |
| Type of collagen | Type I mainly | Type II mainly |
| Proteoglycan | 5%-8% dw | 11%-20% dw |
| Cells | Fusiform | Chondrocytelike |
dw, dry weight.
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.
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.
