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BACKGROUND CONTEXT Painful intervertebral disc degeneration is extremely common and costly. Effective treatments are lacking because the nature of discogenic pain is complex with limited capacity to distinguish painful conditions from age-related changes in the spine. Hypothesized sources of discogenic pain include chronic inflammation, neurovascular ingrowth, and structural disruption. PURPOSE This study aimed to investigate inflammation, pro-neurovascular growth factors, and structural disruption as sources of painful disc degeneration STUDY DESIGN/SETTING This study used an in vivo study to address these hypothesized mechanisms with anterior intradiscal injections of tumor necrosis factor-alpha (TNFα), pro-neurovascular growth factors: nerve growth factor and vascular endothelial growth factor (NGF and VEGF), and saline with additional sham surgery and naïve controls. Depth of annular puncture was also evaluated for its effects on structural and painful degeneration. METHODS Rat lumbar discs were punctured (shallow or deeper puncture) and intradiscally injected with saline, TNFα, or NGF and VEGF. Structural disc degeneration was assessed using X-ray, magnetic resonance imaging (MRI), and histology. The rat painful condition was evaluated using Von Frey hyperalgesia measurements, and substance P immunostaining in dorsal root ganglion (DRG) was performed to determine the source of pain. RESULTS Saline injection increased painful responses with degenerative changes in disc height, MRI intensity, and morphologies of disc structure and cell. TNFα and NGF/VEGF accelerated painful behavior, and TNFα-injected animals had increased substance P in DRGs. Deeper punctures led to more severe disc degeneration. Multiple regression analysis showed that the painful behavior was correlated with disc height loss. CONCLUSIONS We concluded that rate and severity of structural disc degeneration was associated with the amount of annular disruption and puncture depth. The painful behavior was associated with disc height loss and discal inflammatory state, whereas pro-inflammatory cytokines might play a more important role in the level of pain, which might have resulted from enhanced DRG sensitization. These in vivo painful disc degeneration models with different severities of structural changes may be useful for investigating discogenic pain mechanisms and for screening therapies, although interpretations must note the differences between all surgically induced animal models and the human condition.

Study Design Retrospective database analysis. Objective To assess the effect glycemic control has on perioperative morbidity and mortality in patients undergoing elective degenerative lumbar spine surgery. Summary of background data Diabetes Mellitus (DM) is a prevalent disease of glucose dysregulation that has been demonstrated to increase morbidity and mortality following spine surgery. However, there is limited understanding of whether glycemic control influences surgical outcomes in DM patients undergoing lumbar spine procedures for degenerative conditions. Methods The Nationwide Inpatient Sample was analyzed from 2002 to 2011. Hospitalizations were isolated based on International Classification of Diseases Ninth Revision, Clinical Modification procedural codes for lumbar spine surgery and diagnoses codes for degenerative conditions of the lumbar spine. Patients were then classified into three cohorts: controlled diabetics, uncontrolled diabetics and non-diabetics. Patient demographic data, acute complications and hospitalization outcomes were determined for each cohort. Results A total of 403,629 (15.7%) controlled diabetics and 19,421(0.75%) uncontrolled diabetics underwent degenerative lumbar spine surgery from 2002-2011. Relative to non-diabetics, uncontrolled diabetics had significantly increased odds of cardiac complications, deep venous thrombosis and post-operative shock; additionally, uncontrolled diabetics also had an increased mean length of stay (approximately 2.5 days), greater costs (1.3-fold) and a greater risk of inpatient mortality (odds ratio=2.6, 95% confidence interval=1.5-4.8, p < .0009). Controlled diabetics also had increased risk of acute complications and inpatient mortality when compared to non-diabetics, but not nearly to the same magnitude as uncontrolled diabetics. Conclusion Suboptimal glycemic control in diabetic patients undergoing degenerative lumbar spine surgery leads to increased risk of acute complications and poor outcomes. Patients with uncontrolled DM, or poor glucose control, may benefit from improving glycemic control prior to surgery.

The development of an in vivo rodent discogenic pain model can provide insight into mechanisms for painful disc degeneration. Painful disc degeneration in rodents can be inferred by examining responses to external stimuli, observing pain-related behaviors, and measuring functional performance. This study compared the sensitivity of multiple pain and functional assessment methods to disc disruption for identifying the parameters sensitive to painful disc degeneration in rats. Disc degeneration was induced in rats by annular injury with saline injection. The severity of disc degeneration, pain sensitivity, and functional performance were compared to sham and näve control rats. Saline injection induced disc degeneration with decreased disc height and MRI signal intensity as well as more fibrous nucleus pulposus, disorganized annular lamellae and decreased proteoglycan. Rats also demonstrated increased painful behaviors including decreased hindpaw mechanical and thermal sensitivities, increased grooming, and altered gait patterns with hindpaw mechanical hyperalgesia and duration of grooming tests being most sensitive. This is the first study to compare sensitivities of different pain assessment methods in an in vivo rat model of disc degeneration. Hindpaw mechanical sensitivity and duration of grooming were the most sensitive parameters to surgically induced degenerative changes and overall results were suggestive of disc degeneration associated pain.

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