Distal junctional kyphosis in adult cervical deformity patients: where does it occur?

PURPOSE: To evaluate the impact of the lowest instrumented vertebra (LIV) on Distal Junctional kyphosis (DJK) incidence in adult cervical deformity (ACD) surgery. METHODS: Prospectively collected data from ACD patients undergoing posterior or anterior-posterior reconstruction at 13 US sites was reviewed up to 2-years postoperatively (n = 140). Data was stratified into five groups by level of LIV: C6-C7, T1-T2, T3-Apex, Apex-T10, and T11-L2. DJK was defined as a kyphotic increase > 10° in Cobb angle from LIV to LIV-1. Analysis included DJK-free survival, covariate-controlled cox regression, and DJK incidence at 1-year follow-up. RESULTS: 25/27 cases of DJK developed within 1-year post-op. In patients with a minimum follow-up of 1-year (n = 102), the incidence of DJK by level of LIV was: C6-7 (3/12, 25.00%), T1-T2 (3/29, 10.34%), T3-Apex (7/41, 17.07%), Apex-T10 (8/11, 72.73%), and T11-L2 (4/8, 50.00%) (p < 0.001). DJK incidence was significantly lower in the T1-T2 LIV group (adjusted residual = -2.13), and significantly higher in the Apex-T10 LIV group (adjusted residual = 3.91). In covariate-controlled regression using the T11-L2 LIV group as reference, LIV selected at the T1-T2 level (HR = 0.054, p = 0.008) or T3-Apex level (HR = 0.081, p = 0.010) was associated with significantly lower risk of DJK. However, there was no difference in DJK risk when LIV was selected at the C6-C7 level (HR = 0.239, p = 0.214). CONCLUSION: DJK risk is lower when the LIV is at the upper thoracic segment than the lower cervical segment. DJK incidence is highest with LIV level in the lower thoracic or thoracolumbar junction.

Concomitant Posterolateral Corner Injuries in Skeletally Immature Patients With Acute Anterior Cruciate Ligament Injuries.

BACKGROUND: Missed posterolateral corner (PLC) injuries are a known cause of anterior cruciate ligament reconstruction (ACL) failure in the adult population. Failed ACL reconstruction causes significant morbidity in the skeletally immature pediatric population. There is little literature on the character and potential significance of PLC injuries in skeletally immature patients. METHODS: Magnetic resonance imaging studies of the knee at a tertiary care children's hospital for patients who underwent an ACL reconstruction without PLC surgery were retrospectively reviewed. Demographic variables were obtained through chart review, and magnetic resonance imaging studies were evaluated for PLC (popliteus, fibular collateral ligament, popliteofibular ligament, and arcuate ligament) injury, and ACL, medial collateral ligament (MCL), bone bruise, fracture, and meniscal pathology by an experienced pediatric musculoskeletal radiologist. RESULTS: A total of 50 patients with a mean age at 13.3 years at injury were analyzed. PLC injuries were found in 26 patients (52%), with 7 patients (14%) having a complete tear of a component of the PLC. There was no association between sex (P=0.35), Segond fracture (P=0.09), meniscus injury (P=0.92), or MCL injury (P=0.24) with the risk of PLC injury. There was an association between patient age and PLC injury (P=0.02). For each additional year of age, the odds of PLC injury increased by 1.8 times (odds ratio, 1.8; 95% confidence interval, 1.4-2.2). There was no association between PLC injury and ACL graft failure (P=0.19). CONCLUSIONS: Missed PLC injuries are a significant source of morbidity and poor clinical outcomes in the management of concomitant ACL injuries in adults. This study demonstrates the prevalence of PLC injuries in the setting of concomitant ACL injuries in the unique skeletally immature patient population. Incomplete PLC injuries are relatively common. Complete PLC injuries are relatively uncommon. PLC injury was more common in older patients. No other concomitant injury predicted the likelihood of PLC injury. Further research is needed regarding the risk of ACL reconstruction failure from associated PLC injury and the indications for PLC reconstruction in skeletally immature patients. LEVEL OF EVIDENCE: Level IV-diagnostic study.

Molecular Mechanisms of Intervertebral Disc Degeneration.

Intervertebral disc degeneration is a well-known cause of disability, the result of which includes neck and back pain with associated mobility limitations. The purpose of this article is to provide an overview of the known molecular mechanisms through which intervertebral disc degeneration occurs as a result of complex interactions of exogenous and endogenous stressors. This review will focus on some of the identified molecular changes leading to the deterioration of the extracellular matrix of both the annulus fibrosus and nucleus pulposus. In addition, we will provide a summation of our current knowledge supporting the role of associated DNA and intracellular damage, cellular senescence's catabolic effects, oxidative stress, and the cell's inappropriate response to damage in contributing to intervertebral disc degeneration. Our current understanding of the molecular mechanisms through which intervertebral disc degeneration occurs provides us with abundant insight into how physical and chemical changes exacerbate the degenerative process of the entire spine. Furthermore, we will describe some of the related molecular targets and therapies that may contribute to intervertebral repair and regeneration.