Repeated LDH (rLDH), a common complication after lumbar-disc—herniation surgery, is the most common cause of repeated surgery after LDH. The incidence of rLDH is approximately 5.7–15%.[17, 18, 19, 20] The time period for the occurrence of rLDH is currently undefined. One essential condition for a diagnosis of recurrence states that there must be a symptom-free period for a segment of the nerve root before postoperative symptoms appear.[21, 22, 23, 24] Studies show that approximately 60–80% of patients experience recurrent LDH within 6 months after PETD [24, 25, 26]; similar results were obtained in our present study. Therefore, examining the risk factors for early recurrence of LDH after PETD surgery is important for decreasing the incidence of rLDH. Factors that affect the recurrence of LDH after discectomy include: age, sex, body-mass index, occupation, smoking, presence of other comorbidities, segments with intervertebral disc degeneration, number of discs showing degeneration, site of herniation, as well as the type and degree of intervertebral disc degeneration, lumbar vertebral mobility, postoperative exercise intensity, and the learning curve of the operating surgeon; these factors, however, remain debated.[14, 23, 27, 28, 29] Thus far, few studies have reported on the factors influencing early recurrence of LDH after PETD.
Intervertebral disc degeneration is the root cause of LDH. The results obtained in our present study indicate that the risk of developing rLDH increases with the increasing severity of intervertebral disc degeneration, which has also been shown in other studies.[11, 30] During intervertebral disc degeneration, the content of type I collagen increases, while that of type II collagen decreases. Concurrently, proteoglycan and elastin content decreases, causing the nucleus pulposus to lose elasticity and enabling tears in the annulus fibrosus. As intervertebral disc degeneration becomes more severe, the self-repair capacity of annulus fibrosus decreases, leading to nucleus-pulposus herniation.[31]
Sagittal range of motion is a marker used to reflect lumbar vertebral stability. Studies have shown that increased sROM (particularly when sROM >10°) is associated with increased risk of rLDH.[29, 32, 33] sROM is mainly affected by intervertebral disc and facet joints. When sROM increases, instability between lumbar vertebrae, and the resultant stress, may cause rLDH. [30]We found no significant correlation between sROM and rLDH, which may have been due to the low number of patients with early recurrence enrolled in our present study. It is also possible that extension was affected by lumbago during the acquisition of preoperative X-ray images, which were acquired in the extended position.
DHI can objectively reflect intervertebral disc height. One study reported that DHI is a risk factor for rLDH[34, 35]; however, that study did not find that DHI is significantly lower in patients with recurrence compared with those without recurrence, which agreed with the results of Kong.[36] We speculate that this is because increased DHI may provide sufficient space for surgical resection of nucleus pulposus. In addition, Hasegawa theorized that postoperative intervertebral-disc collapse can result in greater intervertebral disc stability.[37] However, our study did not prove that low DHI is a risk factor for rLDH (P=0.076).
Kim et al.[11] found that the risk of recurrence is higher in patients with paracentral herniation than in those with central and far lateral herniation. Conversely, we found that patients with central herniation were more prone to postoperative recurrence than those with paracentral herniation, which agreed with the results of Yao et al.[28] Yin et al.[26] also found that central herniation is an independent risk factor for recurrence after PETD. We believe that this discrepancy may be related to the working positioning of the foraminoscope during the intervertebral-foramen approach used for nucleus-pulposus resection. Therefore, performing this procedure for central herniation using a working cannula will inevitably result in further damage to the annulus fibrosus, which may account for the likely recurrence of central herniation.
Park et al.[24] found that small herniated discs are associated with early recurrence; the smaller the size of the herniated disc, the earlier it recurred. Conversely, we found that patients with increased base-width and postoperative annulus fibrosus tear tended to develop early recurrence after PETD. This may occur because an increased base-width usually indicates that the annulus-fibrosus tear, caused by LDH, is also increased, as is the tendency for residual nucleus pulposus fragmentation during surgery. Hence, to achieve complete decompression, the surgeon may further expand the area for the resection of annulus fibrosus. Annulus-fibrosus tears and defects will accelerate intervertebral disc degeneration, increase the likelihood of nerve-root adhesion and sterile inflammation, and are the main cause of chronic lumbago after discectomy.[38] Lee et al.[25] found that the site of rLDH is generally identical to the original herniation site. This finding indicates that nucleus-pulposus herniation in most rLDH patients is caused by reherniation via the original annulus-fibrosus tear, which may be related to the repair of the annulus-fibrosus tear after PETD. The intervertebral disc is the largest avascular organ in the human body, and its self-repair capacity is limited. Using animal models, Melrose[39] showed that only the outer 1/3 of the annulus-fibrosus tissue can slowly heal using scar formation after damage to the annulus fibrosus. Therefore, a larger tear indicates an increased risk of reherniation at early postoperative stage when the annulus fibrosus has not yet been repaired; this notion is consistent with the results obtained in previous studies.[34, 40, 41] In addition, suturing and repair of the annulus fibrosus during discectomy can effectively decrease the rate of recurrence. [42, 43] This finding also indirectly proves that defects in the annulus fibrosus are associated with recurrence after discectomy.
The results obtained in our present study will aid spinal surgeons in decreasing the recurrence rate of rLDH. Our results indicate that first, relevant radiologic examinations should be completed before surgery. A personalized approach to a surgical procedure should be used if risk factors for postoperative recurrence are discovered. In addition, it is important to implement a postoperative, as well as a 6-month postoperative, follow-up plan for these patients. Second, damage to the annulus fibrosus should be minimized while ensuring complete nerve-root decompression during PETD; this approach is reliant on the surgical techniques used by the surgeon.
Our present study had several limitations. First, the number of patients with early recurrence was low, resulting in statistical limitations stemming from sample size. Second, we only analyzed the relationship between several radiologic factors and early recurrence after PETD, and did not perform a multivariate analysis of epidemiological, anatomical, postoperative-care, and other factors, which may have affected study results. Therefore, a study using detailed statistical analysis will be used in the future to verify the results of our present study.