End-stage extension of the knee and its influence on tibial tuberosity-trochlear groove distance (TTTG) in asymptomatic volunteers

PURPOSE: Increased tibial tuberosity-trochlear groove distance (TTTG) is one potential correcting parameter in patients suffering from lateral patellar instability. It was hypothesized that end-stage extension of the knee might influence the TTTG distance on MR images. METHODS: Transverse T1-weighted MR images of the knee were acquired at full extension, 15° and 30° flexion of the knee in 30 asymptomatic volunteers. MRI parameters: slice thickness: 3 mm, matrix: 256 × 384, FOV: 150 × 150 mm. Two observers independently measured the TTTG at all positions. RESULTS: Mean TTTG for observer 1 was 15.1 ± 3.2 mm at full extension, 10.0 ± 3.5 mm at 15° flexion and 8.1 ± 3.4 mm at 30° flexion. Mean TTTG for observer 2: 14.8 ± 3.3 mm at full extension, 9.4 ± 3.0 mm at 15° flexion, 8.6 ± 3.4 mm at 30° flexion. Mean values were significantly different (p < 0.001) between full extension and 15° as well as 30° flexion for both observers. Mean values were significantly different (p < 0.001) between 15° and 30° for observer 1, but not for observer 2 (n.s.). Interobserver agreement was very good (intraclass correlation coefficient: 0.87-0.88; p < 0.001). CONCLUSIONS: The TTTG increases significantly at the end-stage extension of the knee. Therefore, the comparability of published TTTG values measured on radiographs, CT and MRI at various flexion/extension angles of the knee are limited. LEVEL OF EVIDENCE: Development of diagnostic criteria in a consecutive series of patients and a universally applied 'gold' standard, Level II

Non-Anatomic Proximal Realignment for Recurrent Patellar Dislocation Does Not Sufficiently Prevent Redislocation

Several operative techniques have been described for recurrent patellar dislocation. Clinical results vary depending on the procedure and indication. The present study aimed to evaluate the clinical outcome of Insall’s proximal realignment for recurrent patellar dislocation at mid-term follow-up. Forty-five patients were reviewed with a mean follow-up period of 49 months after having undergone Insall’s procedure. Outcome measures included reports of redislocations, complications, patient-reported outcome scores (Kujala, Tegner activity scale) and subjective assessment. No statistically significant improvements (p < 0.05) in patient-reported outcome measures were noted. Sixteen patients (35%) had poor to fair results using the Kujala score. Subjective assessment revealed that 12 patients (27%) were dissatisfied with the outcome of their surgery and would not undergo the same procedure. Ten patients (22%) had suffered from redislocation at the latest follow-up. In 4 cases (9%), intra-articular knee hematoma occurred which required arthroscopic intervention. The overall mid-term outcome of the present study shows low patient satisfaction. Non-anatomic realignment for recurrent patellar dislocation does not adequately prevent redislocation

Impact of monopolar radiofrequency energy on subchondral bone viability

The purpose of this study was to analyze the impact of monopolar radiofrequency energy treatment on subchondral bone viability. The femoral grooves of six chinchilla bastard rabbits were exposed bilaterally to monopolar radiofrequency energy for 2, 4 and 8 s, creating a total of 36 defects. An intravital fluorescence bone-labeling technique characterized the process of subchondral bone mineralization within the 3 months following exposure to radiofrequency energy and was analyzed by widefield epifluorescence optical sectioning microscopy using an ApoTome. After 2 s of radiofrequency energy exposure, regular fluorescence staining of the subchondral bone was evident in all samples when compared to untreated areas. The depth of osteonecrosis after 4 and 8 s of radiofrequency energy treatment averaged 126 and 942 µm at 22 days (P < .05; P < .01). The 4 s treatment group showed no osteonecrosis after 44 days whereas the depth of osteonecrosis extended from 519 µm at 44 days (P < .01), to 281 µm at 66 days (P < .01) and to 133 µm at 88 days (P < .05) after 8 s of radiofrequency energy application. Though radiofrequency energy may induce transient osteonecrosis in the superficial zone of the subchondral bone, the results of this study suggest that post-arthroscopic osteonecrosis appears to be of only modest risk given the current clinical application in humans

Origin and insertion of the medial patellofemoral ligament: a systematic review of anatomy.

PURPOSE: The medial patellofemoral ligament (MPFL) is the major medial soft-tissue stabiliser of the patella, originating from the medial femoral condyle and inserting onto the medial patella. The exact position reported in the literature varies. Understanding the true anatomical origin and insertion of the MPFL is critical to successful reconstruction. The purpose of this systematic review was to determine these locations. METHODS: A systematic search of published (AMED, CINAHL, MEDLINE, EMBASE, PubMed and Cochrane Library) and unpublished literature databases was conducted from their inception to the 3 February 2016. All papers investigating the anatomy of the MPFL were eligible. Methodological quality was assessed using a modified CASP tool. A narrative analysis approach was adopted to synthesise the findings. RESULTS: After screening and review of 2045 papers, a total of 67 studies investigating the relevant anatomy were included. From this, the origin appears to be from an area rather than (as previously reported) a single point on the medial femoral condyle. The weighted average length was 56 mm with an 'hourglass' shape, fanning out at both ligament ends. CONCLUSION: The MPFL is an hourglass-shaped structure running from a triangular space between the adductor tubercle, medial femoral epicondyle and gastrocnemius tubercle and inserts onto the superomedial aspect of the patella. Awareness of anatomy is critical for assessment, anatomical repair and successful surgical patellar stabilisation. LEVEL OF EVIDENCE: Systematic review of anatomical dissections and imaging studies, Level IV

Human Cytomegalovirus Induces TGF-β1 Activation in Renal Tubular Epithelial Cells after Epithelial-to-Mesenchymal Transition

Human cytomegalovirus (HCMV) infection is associated epidemiologically with poor outcome of renal allografts due to mechanisms which remain largely undefined. Transforming growth factor-β1 (TGF-β1), a potent fibrogenic cytokine, is more abundant in rejecting renal allografts that are infected with either HCMV or rat CMV as compared to uninfected, rejecting grafts. TGF-β1 induces renal fibrosis via epithelial-to-mesenchymal transition (EMT) of renal epithelial cells, a process by which epithelial cells acquire mesenchymal characteristics and a migratory phenotype, and secrete molecules associated with extracellular matrix deposition and remodeling. We report that human renal tubular epithelial cells infected in vitro with HCMV and exposed to TGF-β1 underwent morphologic and transcriptional changes of EMT, similar to uninfected cells. HCMV infected cells after EMT also activated extracellular latent TGF-β1 via induction of MMP-2. Renal epithelial cells transiently transfected with only the HCMV IE1 or IE2 open reading frames and stimulated to undergo EMT also induced TGF-β1 activation associated with MMP-2 production, suggesting a role for these viral gene products in MMP-2 production. Consistent with the function of these immediate early gene products, the antiviral agents ganciclovir and foscarnet did not inhibit TGF-β1 production after EMT by HCMV infected cells. These results indicate that HCMV infected renal tubular epithelial cells can undergo EMT after exposure to TGF-β1, similar to uninfected renal epithelial cells, but that HCMV infection by inducing active TGF-β1 may potentiate renal fibrosis. Our findings provide in vitro evidence for a pathogenic mechanism that could explain the clinical association between HCMV infection, TGF-β1, and adverse renal allograft outcome

Structure of the mouse glial fibrillary acidic protein gene: implications for the evolution of the intermediate filament multigene family.

We report the complete sequence of the gene encoding mouse glial fibrillary acidic protein (GFAP), the intermediate filament (IF) protein specific to astrocytes. The 9.8 kb gene includes nine exons separated by introns ranging in size from 0.2 to 2.5 kb. A comparison of the organization of the GFAP gene with that of genes encoding other IF proteins reveals that the structure of IF genes is highly conserved in spite of considerable divergence at the amino acid level. Thus, most of the evolutionary events leading to the placement of introns in IF genes must have occurred prior to the duplication and subsequent divergence of IF genes from a presumptive common ancestral sequence. The conserved gene organization is unrelated to structural features of IF proteins. A curious feature of the GFAP gene is the large number of repeated sequences found in the introns. Six tracts of reiterated di- or trinucleotides are present, plus tandem repeats of two different novel sequences. One repeat is unique to the GFAP gene; the other occurs elsewhere in the mouse genome, although at relatively low frequency