The role of elbow positioning on arthroscopic assessment of the long head of biceps tendon in the beach chair position.

BACKGROUND: Tendinopathy of the long head of biceps (LHB) tendon is a common cause of anterior shoulder pain and dysfunction. The extra-articular portion within the bicipital groove undergoes frequent load and friction during shoulder movements and pathology within this area is frequently missed during arthroscopic assessment. METHODS: We quantified the arthroscopically assessable length of tendon within the shoulder in 14 consecutive patients undergoing subpectoral biceps tenodesis. After biceps tenotomy at the superior labrum, the tagged tendon was maximally tensioned and marked at the biceps outlet with the elbow in extension and flexion. The distance in distance between the two were measured. RESULTS: Mean distance from the superior labral insertion of the biceps to the outlet was 16.4 ± 4.1 mm (range, 11-25). With tension on the biceps with elbow extension, the mean measurable distance was 31.3 ± 6.7 mm (range, 19-45). With elbow flexion, this increased to 39.5 ± 5.9 mm (range, 25-52). Mean increase in visible tendon length was 8.2 ± 4.3 mm (range, 5-21) (p = 0.002). CONCLUSION: Elbow flexion results in an average increase of 26.2% more extra-articular tendon visualized at arthroscopy. Therefore, we believe that elbow flexion is a useful adjunct, especially when performed in conjunction with techniques that pull the tendon into the joint, thus allowing for more complete arthroscopic assessment of the LHB, increasing detection of symptomatic biceps tendonitis. LEVEL OF EVIDENCE: Level IV.

Glenoid vault perforation in total shoulder arthroplasty: Do we need computer guidance?

The proliferation of computer 3D simulation and computer-generated guides is aimed at minimizing perforation of the glenoid vault by glenoid pegs in shoulder arthroplasty, based on assumptions that perforation leads to worse outcomes by component loosening and potential failure. We evaluated outcomes of glenoid peg perforation testing the assumption that perforation produces worse results. Eighty-three shoulders underwent shoulder arthroplasty with pegged hybrid fixation (bone-ingrowth flanged central glenoid peg and peripheral cemented pegs) without precision signal injector guides or use of 3D planning software. Outcomes were determined by American Shoulder and Elbow Score and Oxford Shoulder Score. Fine slice CT determined the presence of vault perforation and the extent of lucent lines at the prosthesis-bone interface and bony morphology of the vault perforation. Follow-up was 46.7 months (24-99). Seven shoulders (8%) demonstrated perforation of glenoid vault. Bony ingrowth and cortical overgrowth occurred despite perforation, with no clinically significant differences in clinical or radiological outcomes in shoulders with and without glenoid vault perforation. None of these patients underwent revision surgery. Despite not utilizing computer planning and/or guides, 92% of implants did not perforate the glenoid vault. However, glenoid vault perforation in our series produced excellent outcomes with no increased risk of revision as a result of glenoid vault perforation.

Characterization of the Proximal Long Head of Biceps Tendon Anatomy Using Magnetic Resonance Imaging: Implications for Biceps Tenodesis.

BACKGROUND: Biceps tenodesis is a common treatment for proximal long head of biceps (LHB) tendon pathology. To maintain biceps strength and contour and minimize cramping, restoration of muscle-length tension and appropriate positioning of the tenodesis is key. Little is known about the biceps musculotendinous junction (MTJ) anatomy, especially in relation to the overlying pectoralis major tendon (PMT), which is a commonly used landmark for tenodesis positioning. PURPOSE: To characterize the in vivo topographic anatomy of the LHB tendon, in particular the MTJ relative to the PMT, using a novel axial proton-density magnetic resonance imaging (MRI) sequence. STUDY DESIGN: Descriptive laboratory study. METHODS: In total, 45 patients having a shoulder MRI for symptoms unrelated to their biceps tendon or rotator cuff were prospectively recruited. There were 33 men and 12 women, with a mean age of 37 ± 13 years (range, 18-59 years). All patients underwent routine shoulder MRI scans with an additional axial proton density sequence examining the LHB tendon and its MTJ. Three independent observers reviewed each MRI scan, and measurements were obtained for (1) MTJ length, (2) the distance between the proximal MTJ and the superior border of the PMT (MTJ-S), (3) the distance between the distal MTJ to the inferior border of the PMT, and (4) the width of the PMT. RESULTS: The average position of the MTJ-S was 5.9 ± 10.8 mm distal to the superior border of the PMT. The mean MTJ length was 32.5 ± 8.3 mm and the width of the PMT was 28.0 ± 7.3 mm. We found no significant correlation between patient age, height, sex, or body mass index and any of the biceps measurements. We observed wide variability of the MTJ-S position and identified 3 distinct types of biceps MTJ: type 1, MTJ-S above the PMT; type 2, MTJ-S between 0 and 10 mm below the superior border of the PMT; and type 3, MTJ-S >10 mm distal to the superior PMT. CONCLUSION: In this study, the in vivo anatomy of the LHB tendon is characterized relative to the PMT using a novel MRI sequence. The results demonstrate wide variability in the position of the MTJ relative to the PMT, which can be classified into 3 distinct subtypes or zones relative to the superior border of the PMT. Understanding this potentially allows for accurate and anatomic placement of the biceps tendon for tenodesis. CLINICAL RELEVANCE: To our knowledge, this is the first study to radiologically analyze the in vivo topographic anatomy of the LHB tendon and its MTJ. The results of this study provide more detailed understanding of the variability of the biceps MTJ, thus allowing for more accurate placement of the biceps tendon during tenodesis.

Minimizing Propionibacterium acnes contamination in shoulder arthroplasty: use of a wound protector.

BACKGROUND: Propionibacterium acnes may be transmitted from the subdermal tissues to the deeper tissues during shoulder arthroplasty surgery, resulting in deep infection. The aim of this prospective, clinical study was to determine whether the use of a wound protector drape can lower the incidence of P. acnes in the wound during shoulder arthroplasty surgery. METHODS: For a consecutive series of 47 patients undergoing shoulder arthroplasty, a wound protector drape was used during surgery, to isolate the subdermal layer from the surgeons' hands, retractors and other instruments. Microbiological swabs were taken both from the subdermal layer and the exposed drape to determine the incidence of P. acnes at both sites. RESULTS: The overall incidence of P. acnes in the subdermal layer was 23%. A fivefold decrease in the incidence of P. acnes in the exposed superficial layer was demonstrated by use of the wound protector drape. CONCLUSION: Use of a wound protector drape to isolate the superficial tissue layer from the surgeons' gloves, instruments and retractors decreases the incidence of P. acnes in the surgical field. This may result in a decreased rate of transmission to the deeper tissues, and a decreased rate of P. acnes deep infection.

Cohesion fatigue induces chromatid separation in cells delayed at metaphase.

BACKGROUND: Chromosome instability is thought to be a major contributor to cancer malignancy and birth defects. For balanced chromosome segregation in mitosis, kinetochores on sister chromatids bind and pull on microtubules emanating from opposite spindle poles. This tension contributes to the correction of improper kinetochore attachments and is opposed by the cohesin complex that holds the sister chromatids together. Normally, within minutes of alignment at the metaphase plate, chromatid cohesion is released, allowing each cohort of chromatids to move synchronously to opposite poles in anaphase, an event closely coordinated with mitotic exit. RESULTS: Here we show that during experimentally induced metaphase delay, spindle pulling forces can cause asynchronous chromatid separation, a phenomenon we term "cohesion fatigue." Cohesion fatigue is not blocked by inhibition of Plk1, a kinase essential for the "prophase pathway" of cohesin release from chromosomes, or by depletion of separase, the protease that normally drives chromatid separation at anaphase. Cohesion fatigue is inhibited by drug-induced depolymerization of mitotic spindle microtubules and by experimentally increasing the levels of cohesin on mitotic chromosomes. In cells undergoing cohesion fatigue, cohesin proteins remain associated with the separated chromatids. CONCLUSION: In cells arrested at metaphase, pulling forces originating from kinetochore-microtubule interactions can, with time, rupture normal sister chromatid cohesion. This cohesion fatigue, resulting in unscheduled chromatid separation in cells delayed at metaphase, constitutes a previously overlooked source for chromosome instability in mitosis and meiosis.

Mitotic progression becomes irreversible in prometaphase and collapses when Wee1 and Cdc25 are inhibited.

Mitosis requires precise coordination of multiple global reorganizations of the nucleus and cytoplasm. Cyclin-dependent kinase 1 (Cdk1) is the primary upstream kinase that directs mitotic progression by phosphorylation of a large number of substrate proteins. Cdk1 activation reaches the peak level due to positive feedback mechanisms. By inhibiting Cdk chemically, we showed that, in prometaphase, when Cdk1 substrates approach the peak of their phosphorylation, cells become capable of proper M-to-G1 transition. We interfered with the molecular components of the Cdk1-activating feedback system through use of chemical inhibitors of Wee1 and Myt1 kinases and Cdc25 phosphatases. Inhibition of Wee1 and Myt1 at the end of the S phase led to rapid Cdk1 activation and morphologically normal mitotic entry, even in the absence of G2. Dampening Cdc25 phosphatases simultaneously with Wee1 and Myt1 inhibition prevented Cdk1/cyclin B kinase activation and full substrate phosphorylation and induced a mitotic "collapse," a terminal state characterized by the dephosphorylation of mitotic substrates without cyclin B proteolysis. This was blocked by the PP1/PP2A phosphatase inhibitor, okadaic acid. These findings suggest that the positive feedback in Cdk activation serves to overcome the activity of Cdk-opposing phosphatases and thus sustains forward progression in mitosis.