Degenerative disc disease (DDD) is a common cause of lower back pain. Calcification of the intervertebral disc (IVD) has been correlated with DDD, and is especially prevalent in scoliotic discs. The appearance of calcium deposits has been shown to increase with age, and its occurrence has been associated with several other disorders such as hyperparathyroidism, chondrocalcinosis, and arthritis. Trauma, vertebral fusion and infection have also been shown to increase the incidence of IVD calcification. Our data indicate that Ca²⁺ and expression of the extracellular calcium-sensing receptor (CaSR) are significantly increased in mild to severely degenerative human IVDs. In this study, we evaluated the effects of Ca²⁺ and CaSR on the degeneration and calcification of IVDs.

Human donor lumbar spines of Thompson grade 2, 3 and 4 through organ donations within 24 hs after death. IVD cells, NP and AF, were isolated from tissue by sequential digestion with Pronase followed by Collagenase. Cells were expanded for 7 days under standard cell culture conditions. Immunohistochemistry was performed on IVD tissue to validate the grade and expression of CaSR. Free calcium levels were also measured and compared between grades. Immunocytochemistry, Western blotting and RT-qPCR were performed on cultured NP and AF cells to demonstrate expression of CaSR, matrix proteins aggrecan and collagen, catabolic enzymes and calcification markers. IVD cells were cultured in increasing concentrations of Ca²⁺ [1.0-5.0 mM], CaSR allosteric agonist (cincalcet, 1 uM), and IL-1b [5 ng/mL] for 7 days. Ex vivo IVD organ cultures were prepared using PrimeGrowth Disc Isolation System (Wisent Bioproducts, Montreal, Quebec). IVDs were cultured in 1.0, 2.5 mM Ca²⁺ or with cinacalcet for 21 days to determine effects on disc degeneration, calcification and biomechanics. Complex modulus and structural stiffness of disc tissues was determined using the MACH-1 mechanical testing system (Biomomentum, Laval, Quebec).

Ca²⁺ dose-dependently decreased matrix protein synthesis of proteoglycan and Col II in NP and AF cells, similar to treatment with IL-1b. (n = 4). Contrarily to IL-1b, Ca²⁺ and cincalcet did not significantly increase the expression of catabolic enzymes save ADAMTS5. Similar effects were observed in whole organ cultures, as Ca²⁺ and cinacalcet decreased proteoglycan and collagen content. Although both Ca²⁺ and cinacalcet increased the expression of alkaline phosphatase (ALP), only in Ca²⁺-treated IVDs was there evidence of calcium deposits in NP and AF tissues as determined by von Kossa staining. Biomechanical studies on Ca²⁺ and cinacalcet-treated IVDs demonstrated decreases in complex modulus (p<0.01 and p<0.001, respectively; n=5), however, only Ca²⁺-treated IVDs was there significant increases stiffness in NP and AF tissues (p<0.001 and p<0.05, respectively; n=3).

Our results suggest that changes in the local concentrations of calcium and activation of CaSR affects matrix protein synthesis, calcification and IVD biomechanics. Ca²⁺ may be a contributing factor in IVD degeneration and calcification.

Our study is still in progress. The results mentioned in the abstract are preliminary results. The final results will be provided at the time of presentation.

Over the past decade, the widespread availability of high-resolution ultrasonography coupled with advances in regional anaesthesia have popularised peripheral nerve blocks for anterior cruciate ligament reconstructions (ACLRs). The aim of this study is to investigate whether the femoral nerve block (FNB) administered at the time of ACLR has any long-term impact on the quadriceps strength as compared to patients who did not receive a FNB.

This is a retrospective study. Four hundred charts of patients who underwent ACLR at our institution and had subsequent Biodex testing (an isokinetic rehabilitation test that provides objective information about muscle strength deficits and imbalances of the operated leg compared to the non-operated leg) from 2004 to 2015 were reviewed. Patients who had prior ipsilateral knee surgery, multi-ligament knee injury or at extreme ages were excluded from the study. The following baseline patient characteristics was recorded for each reviewed chart: age, sex, medical comorbidities, the date of the injury, date of the surgery, surgery technical notes and associated procedures, the surgeon, the hospital were the patient was operated, the Biodex test date and the Biodex test results. Data extraction assessed any association between the ACLR patients' who received FNB with the results of the Biodex test after completing the rehabilitation protocol. Descriptive statistics were used to compare the type of anaesthesia, mode of pain control and the results of the Biodex tests between patients grouped by the mode of anaesthesia used at the time of surgery (FNB versus no FNB). A multivariate regression model then compared quadriceps strength (inferred by Biodex test results) between groups while controlling for baseline differences between groups.

Fifty five percent of the ACLR patients received FNB compared to 45% that did not receive FNB over the last 11 years of performing ACLRs (2004–2015) at our institute. Fifty percent of the patients that received FNB failed to achieve more than or equal to 80% quadriceps strength (compared to the contralateral non-operated leg) at 6 months on Biodex test. On the other hand, only 20% of the non-FNB group failed to achieve more than or equal to 80% quadriceps strength.

This study lead us to think that ACLR patients that received FNB are significantly weaker in quadriceps strength at 6 months post ACLR in comparison to non-FNB ACLR patients. This finding subsequently might affect the time needed to return to sports and might indicate a considerable clinical consequence of the FNB on ACL-reconstruction patients.