Background: Certain failures of arthroscopic Bankart repairs seem to be related to the presence of a Hill-Sachs defect. It has been suggested that Hill-Sachs lesions can be treated by “remplissage” (filling in) of the defect. The effect of this procedure on the mobility of the shoulder is not known. Purpose: To determine if filling in the Hill-Sachs defect with rotator cuff tendon would modify the range of motion of the operated shoulder. Study Design: Cohort study; Level of evidence, 2. Methods: A prospective study of 2 patient populations (arthroscopic Bankart repair alone vs Bankart and remplissage) was undertaken after selecting patients using the Instability Severity Index Score (ISIS). Patients with a Hill-Sachs lesion seen on anteroposterior radiographs had a remplissage procedure if this procedure allowed them to obtain an ISIS lower than 4. The main clinical outcome was the range of motion (external rotation at the side [ER1], external rotation in abduction [ER2], internal rotation [IR], and forward elevation), assessed by the difference between each shoulder at 1 and 2 years’ follow-up. Complications, recurrence, and the Walch-Duplay scores were noted at the same time. Minimum follow-up was 2 years. Results: No significant statistical difference was noted in the range of motion between each group: ER1, difference of 4° (P = .22); ER2, difference of 3° (P = .49); anterior elevation, difference of 5° (P = .35); and internal rotation, 2 vertebrae (P = .22). The rate of recurrence was identical in both groups (6.25%). For patients without redislocation, the Walch-Duplay score was excellent (14/17) or good (3/17) in the first group and excellent (12/15) or good (3/15) in the second group. Posterosuperior pain during forceful movements or when tired was noted in one third of patients having undergone remplissage. Conclusion: The remplissage technique did not alter the range of motion of the shoulder compared with Bankart procedure alone; however, one third of patients did experience posterosuperior pain.

Introduction: Visfatin is an adipokine that may be involved in intertissular joint communication in osteoarthritis (OA). With a homodimeric conformation, it exerts nicotinamide phosphoribosyltransferase (Nampt) enzymatic activity, essential for nicotinamide adenine dinucleotide biosynthesis. We examined the tissular origin and conformation of visfatin/Nampt in human OA joints and investigated the role of visfatin/Nampt in chondrocytes and osteoblasts by studying Nampt enzymatic activity. Methods: Synovium, cartilage and subchondral bone from human OA joints were used for protein extraction or incubated for 24 hours in serum-free media (conditioned media), and synovial fluid was obtained from OA patients. Visfatin/Nampt expression in tissular extracts and conditioned media was evaluated by western blot and enzyme-linked immunosorbent assay (ELISA), respectively. Nampt activity was assessed in OA synovium by colorimetric assay. Primary cultures of murine chondrocytes and osteoblasts were stimulated with visfatin/Nampt and pretreated or not with APO866, a pharmacologic inhibitor of Nampt activity. The effect on cytokines, chemokines, growth factors and hypertrophic markers expression was examined by quantitative reverse transcriptase polymerase chain reaction and/or ELISA. Results: In tissular explants, conditioned media and synovial fluid, visfatin/Nampt was found as a homodimer, corresponding to the enzymatically active conformation. All human OA joint tissues released visfatin/Nampt (synovium: 628 ± 106 ng/g tissue; subchondral bone: 195 ± 26 ng/g tissue; cartilage: 152 ± 46 ng/g tissue), with significantly higher level for synovium (P <0.0005). Nampt activity was identified ex vivo in synovium. In vitro, visfatin/Nampt significantly induced the expression of interleukin 6, keratinocyte chemoattractant and monocyte chemoattractant protein 1 in chondrocytes and osteoblasts. APO866 decreased the mRNA and protein levels of these pro-inflammatory cytokines in the two cell types (up to 94% and 63% inhibition, respectively). Levels of growth factors (vascular endothelial growth factor, transforming growth factor β) and hypertrophic genes were unchanged with treatment. Conclusion: Visfatin/Nampt is released by all human OA tissues in a dimeric enzymatically active conformation and mostly by the synovium, which displays Nampt activity. The Nampt activity of visfatin is involved in chondrocyte and osteoblast activation, so targeting this enzymatic activity to disrupt joint tissue interactions may be novel in OA therapy.