disease (DDD) is a highly desirable objective. Such a treatment would need to provide anti-catabolic, pro-anabolic and anti-inflammatory ef- fects on the intervertebral disc (IVD). In particular, stabilization of ex- tracellular matrix (ECM) within the nucleus pulposus (NP) and maintenance of the healthy NP cellular phenotype would be important goals. Here we demonstrate that conditioned medium developed from the notochordal cell (NC)-rich non-chondrodystrophic (NCD) canine NP (‘‘NCCM’’) can rescue degeneration of the IVD in a preclinical rat-tail model of DDD. PURPOSE: To determine ability of a single injection of NCCM to regen- erate the IVD NP in a preclinical model of rat-tail disc induced DDD. STUDY DESIGN/SETTING: In vivo quantitative biochemical/molecular study. OUTCOME MEASURES: Immunohistochemistry and Western blotting. METHODS: We induced DDD in 12-week old female Wistar rat-tails us- ing a fluoroscopically guided, 26G needle puncture injury within the prox- imal four caudal discs. At 4 weeks postinjury, we injected 8ml of NCCM into the injured discs of five animals or equal volumes of PBS in five con- trol animals. We humanely euthanized the animals at 10 weeks postinjury and evaluated the effects of NCCM using immunohistochemistry (IHC) and Western blotting for proteins of interest. We assessed the expression of markers of NC cells (brachyury and galectin-3), chondrocyte-like-cells (CLCs) (carbonic anhydrase XII, Sox9), extracellular matrix (ECM) and ECM remodeling molecules (collagen II, MMP- 13), pro-inflammatory markers (active form of IL-1b and Cox2), signaling proteins (NFkb and b-catenin), and stem cell markers Oct3/4 and Nanog. We verified our West- ern blotting with IHC. RESULTS: At 10 weeks postinjury the NCCM-treated discs revealed a marked regenerative response compared to controls where the expression of the inflammatory markers IL-1b subunit (active form) and COX2 were undetectable, suggesting that NCCM confers a strong anti-inflammatory effect on the NP. Markers of NCs (brachyury and galectin-3) and stem- ness (Nanog and Oct3/4) are also preserved and there is an increase in the expression of b-catenin. There was also an increase in the expression of collagen type II and Sox9, demonstrative that NCCM induces an ana- bolic effect on the NP ECM. On the other hand, PBS-treated rat-tail discs assume a degenerative, fibrocartilaginous metaplasia-like phenotype. These discs display a loss of NC and stem cell markers, increased ex- pression of CLCs, and a marked increase in the active form of the in- flammatory markers IL-1b and COX2 as well as increased MMP-13 expression. CONCLUSIONS: For the first time we demonstrate that a single injec- tion of NCCM can restore the healthy cellular phenotype of the degener- ative disc and demonstrate anabolic effects on the NP ECM. The necessary and sufficient factors contained within NCCM could be har- nessed within a minimally invasive biological therapy for the treatment of DDD. FDA DEVICE/DRUG STATUS: This abstract does not discuss or include any applicable devices or drugs. http://dx.doi.org/10.1016/j.spinee.2015.07.128 103. Interrelationships of Vitamin D Status, Bone Health and Fusion Consolidation Ruben Maldonado, BS 1 , Mark Svet 2 , Lea Kanim, MA 3 , Melodie F. Metzger, PhD 4 ; 1 Orthopaedic Biomechanics Laboratory, Los Angeles, CA, US; 2 Brea, CA, US; 3 Spine Center, Cedars-Sinai Medical Center, Los Angeles, CA, US; 4 Cedars Sinai Medical Center, West Hollywood, CA, US BACKGROUND CONTEXT: A growing number of reports demonstrate alarming rates of inadequate serum vitamin D levels in orthopedic patients. While it is known that vitamin D plays an important role in overall skeletal health and disease prevention, its significance to bone health during frac- ture healing remains inconclusive. PURPOSE: This study reports interrelationships among geometry, density and biomechanics of the femur as proxy measures for bone health to stiff- ness and consolidation of spinal fusion in normal rats exposed to experi- mentally manipulated dietary vitamin D. STUDY DESIGN/SETTING: Prospective, in vivo study, with serum vita- min D follow-up, with experimentally adjusted dietary vitamin D, in rats having undergone posterolateral fusion with tail bone autograft. PATIENT SAMPLE: 48 male Sprague Dawley rats. OUTCOME MEASURES: Biomechanical stiffness of femur and spine, microCT density and volumetric measures of femur and spine, microCT geometry measures of femur, bone mineral content of femur (ashing). METHODS: 48 male Sprague Dawley rats were randomized into 4 diet- ary vitamin D groups: 0 IU/g vitamin D, 2.25 IU/g vitamin D, 5 IU/g vi- tamin D, and 40 IU/g vitamin D. Dietary calcium was maintained at normal levels across the diets. Plasma was collected and 25(OH)D and cal- cium levels were determined via radioimmunoassay. Rats underwent post- erolateral spinal fusion surgery with autogenous tail grafting. After 16 weeks, rats were sacrificed for femur and spinal fusion evaluation. Mi- croCT analysis was performed for bone geometric and density measures. Three-point bending tests were performed on the femur to measure stiff- ness and strength. Femur specimens were ashed to determine bone mineral content. RESULTS: Serum levels of vitamin D were significantly associated with levels of vitamin D adjusted chow. Serum Ca was also related to dietary vitamin D. Serum vitamin D decreased during the spine healing interval, from postoperative collection to sacrifice. Femur microCT geometric var- iables including cross-sectional area, inertia and bone volume were signifi- cantly related to vitamin D. Spine microCT density measures were significantly related to dietary vitamin D while femur microCT density measures were not related to vitamin D. Femur stiffness and strength were both significantly correlated to dietary and serum vitamin D, and stiffness and strength were intra-correlated. CONCLUSIONS: Quantitative measures of overall bone health were as- sociated with increasing levels of vitamin D and calcium, which trans- lated to trends in enhanced consolidation in spinal fusion. Vitamin D affected femur stiffness to a greater extent than spinal stiffness after a spinal fusion procedure. Potentially, high cancellous bone volume in the spinal fusion site during the remodeling process increased irregularity of bone architectural makeup inducing development of stress concentra- tion points that increased stiffness data variability. Also, it is possible that in deficient or inadequate vitamin D intake, low availability of vitamin D in the blood increases demand of resorption in native bone as was evident by the positive association of femur bone volume to vitamin D. Conse- quently, vitamin D was found to be more highly associated with femur biomechanical stiffness. The results herein provide quantitative data on femora bone quality of the host after spinal fusion healing as a function of manipulated dietary vitamin D status in rats. Our results indicate vita- min D affects overall bone health and to a lesser extent affects bone heal- ing, as in spinal fusion. Thus, treating hypovitaminosis D is prominently important for bone health as well as enhancing bone formation and healing. FDA DEVICE/DRUG STATUS: This abstract does not discuss or include any applicable devices or drugs. http://dx.doi.org/10.1016/j.spinee.2015.07.129 104. Effect of rhBMP-2 on Lung Cancer Spine Metastasis in Rodents Abhishek Kannan, BS 1 , Kevin A. Sonn, MD 2 , Sharath S. Bellary, MD, MS 3 , Chawon Yun, PhD 3 , Sohaib Hashmi, MD 1 , Ralph Cook 3 , Amruta Ashtekar 4 , Anjan Ghosh 1 , Michael S. Nickoli, MD 5 , Jason H. Ghodasra, MD 6 , Michael Okoli, BA 5 , Stuart R. Stock, PhD 1 , Erin L. Hsu, PhD 3 , Wellington K. Hsu, MD 3 ; 1 Northwestern Feinberg School of Medicine Department of Orthopaedic Surgery, Chicago, IL, US; 2 Maywood, IL, US; 3 Northwestern University, Chicago, IL, US; 134S Proceedings of the NASS 30th Annual Meeting / The Spine Journal 15 (2015) 87S–267S Refer to onsite Annual Meeting presentations and postmeeting proceedings for possible referenced figures and tables. Authors are responsible for accurately reporting disclosures and FDA device/drug status at time of abstract submission.