Arthroscopic classification of posterior labrum glenoid insertion

AbstractPurposeWe performed a prospective arthroscopic study to explore the variability of the posterior labrum glenoid insertion. We aimed to classify the insertions and to explore whether these insertions can be identified by pre-operative arthro-CT scan.Patients and methodsFrom January to December 2011, 86 patients were prospectively included in the current study. During arthroscopy, anterior labrum was evaluated and posterior labrum was assessed in 3 different locations: superior, medial, and inferior. For each segment, the labrum was considered normally inserted (directly to the glenoid cartilage), medialized (inserted at the posterior part of the glenoid bone, without direct contact with the cartilage), torn (macroscopic degenerative changes, tears, fragments) or absent (agenesis). Imaging was analyzed segment by segment by an experienced osteoarticular radiologist, using the same classification.ResultsFour types of posterior labrum insertions were identified. Type 1, 60% of the cases, corresponded to a posterior labrum totally inserted in the glenoid, with direct contact with the cartilage. Type 2, 20% of the cases, represented medialized insertion of the superior segment. Type 3, 15% of the cases, represented an associated medialization of the superior and medial segment of the posterior labrum. Type 4 is a medialized insertion of the all-posterior labrum. Fifty-six shoulders were used for arthro-CT and arthroscopy correlation: for the superior segment (n=22/56), the sensitivity of arthro-CT to identify an abnormal insertion when the labrum is medialized was 68.18%, specificity 70.59%, positive predictive value (PPV) 60%, and negative predictive value (NPV) 77.42%. For the medial segment (n=16/56), the sensitivity of arthro-CT to identify an abnormal insertion when the labrum is medialized was 81.25%, specificity 57.50%, PPV 43.33% and NPV 88.46%. For the inferior segment (n=5/56), the sensitivity was 100%, specificity 47.60%, PPV 15.63% and NPV 100%.ConclusionThe current study points out the high variability of shoulder posterior labrum glenoid insertion, and thus the risk of misdiagnosis with posterior labral tears, especially in posterior instability and also the risk of considering as labral lesions some non-pathological aspects.Level of evidenceLevel III. Anatomic prospective study

Uncovering the effect of low-frequency static magnetic field on tendon-derived cells: from mechanosensing to tenogenesis

Magnetotherapy has been receiving increased attention as an attractive strategy for modulating cell physiology directly at the site of injury, thereby providing the medical community with a safe and non- invasive therapy. Yet, how magnetic eld in uences tendon cells both at the cellular and molecular levels remains unclear. Thus, the in uence of a low-frequency static magnetic eld (2 Hz, 350 mT) on human tendon-derived cells was studied using di erent exposure times (4 and 8 h; short-term studies) and di erent regimens of exposure to an 8h-period of magnetic stimulation (continuous, every 24 h or every 48 h; long-term studies). Herein, 8 h stimulation in short-term studies signi cantly upregulated the expression of tendon-associated genes SCX, COL1A1, TNC and DCN (p < 0.05) and altered intracellular Ca2+ levels (p < 0.05). Additionally, every 24 h regimen of stimulation signi cantly upregulated COL1A1, COL3A1 and TNC at day 14 in comparison to control (p < 0.05), whereas continuous exposure di erentially regulated the release of the immunomodulatory cytokines IL-1β and IL-10 (p < 0.001) but only at day 7 in comparison to controls. Altogether, these results provide new insights on how low-frequency static magnetic eld ne-tune the behaviour of tendon cells according to the magnetic settings used, which we foresee to represent an interesting candidate to guide tendon regeneration.info:eu-repo/semantics/publishedVersio

Mesenchymal Stem Cell Therapy Regenerates the Native Bone-Tendon Junction after Surgical Repair in a Degenerative Rat Model

BACKGROUND: The enthesis, which attaches the tendon to the bone, naturally disappears with aging, thus limiting joint mobility. Surgery is frequently needed but the clinical outcome is often poor due to the decreased natural healing capacity of the elderly. This study explored the benefits of a treatment based on injecting chondrocyte and mesenchymal stem cells (MSC) in a new rat model of degenerative enthesis repair. METHODOLOGY: The Achilles' tendon was cut and the enthesis destroyed. The damage was repaired by classical surgery without cell injection (group G1, n = 52) and with chondrocyte (group G2, n = 51) or MSC injection (group G3, n = 39). The healing rate was determined macroscopically 15, 30 and 45 days later. The production and organization of a new enthesis was assessed by histological scoring of collagen II immunostaining, glycoaminoglycan production and the presence of columnar chondrocytes. The biomechanical load required to rupture the bone-tendon junction was determined. PRINCIPAL FINDINGS: The spontaneous healing rate in the G1 control group was 40%, close to those observed in humans. Cell injection significantly improved healing (69%, p = 0.0028 for G2 and p = 0.006 for G3) and the load-to-failure after 45 days (p<0.05) over controls. A new enthesis was clearly produced in cell-injected G2 and G3 rats, but not in the controls. Only the MSC-injected G3 rats had an organized enthesis with columnar chondrocytes as in a native enthesis 45 days after surgery. CONCLUSIONS: Cell therapy is an efficient procedure for reconstructing degenerative entheses. MSC treatment produced better organ regeneration than chondrocyte treatment. The morphological and biomechanical properties were similar to those of a native enthesis

Prion Protein Is a Key Determinant of Alcohol Sensitivity through the Modulation of N-Methyl-D-Aspartate Receptor (NMDAR) Activity

The prion protein (PrP) is absolutely required for the development of prion diseases; nevertheless, its physiological functions in the central nervous system remain elusive. Using a combination of behavioral, electrophysiological and biochemical approaches in transgenic mouse models, we provide strong evidence for a crucial role of PrP in alcohol sensitivity. Indeed, PrP knock out (PrP−/−) mice presented a greater sensitivity to the sedative effects of EtOH compared to wild-type (wt) control mice. Conversely, compared to wt mice, those over-expressing mouse, human or hamster PrP genes presented a relative insensitivity to ethanol-induced sedation. An acute tolerance (i.e. reversion) to ethanol inhibition of N-methyl-D-aspartate (NMDA) receptor-mediated excitatory post-synaptic potentials in hippocampal slices developed slower in PrP−/− mice than in wt mice. We show that PrP is required to induce acute tolerance to ethanol by activating a Src-protein tyrosine kinase-dependent intracellular signaling pathway. In an attempt to decipher the molecular mechanisms underlying PrP-dependent ethanol effect, we looked for changes in lipid raft features in hippocampus of ethanol-treated wt mice compared to PrP−/− mice. Ethanol induced rapid and transient changes of buoyancy of lipid raft-associated proteins in hippocampus of wt but not PrP−/− mice suggesting a possible mechanistic link for PrP-dependent signal transduction. Together, our results reveal a hitherto unknown physiological role of PrP on the regulation of NMDAR activity and highlight its crucial role in synaptic functions