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Background: The purpose of this study was to determine the intra- and inter-rater reliability of detecting full- and partial-thickness tears of the supraspinatus intramuscular central tendon on magnetic resonance imaging (MRI) by orthopaedic shoulder surgeons. Full-thickness tears of this tendon have previously been associated with the failure of nonsurgical management of rotator cuff tears. Methods: Shoulder MRIs from 40 patients entered into a prospective rotator cuff disease database were independently reviewed by two musculoskeletal (MSK) radiologists in order to determine if there was a partial- or full-thickness tear of the supraspinatus central tendon. The MRIs were randomly sorted and distributed to 16 fellowship-trained shoulder surgeons. The surgeons then similarly diagnosed each patient. After a 1-month interval, surgeons repeated the evaluation with the same set of randomly reordered MRIs. Surgeon intra- and inter-rater reliability was determined with the kappa statistic. Agreement and inter-rater reliability were also determined between the shoulder surgeons and MSK radiologists. Results: For full-thickness tears, the intra-rater reliability was excellent (0.86 ± 0.1, 95% confidence interval (CI): 0.81, 0.91) and the agreement was 93.4% ± 4.6, 95% CI: 91.1, 95.8. Inter-rater reliability for both rounds was also excellent (0.77 and 0.74). The agreement between the shoulder surgeons and MSK radiologists was 92.9% ± 3.9, 95% CI: 90.9, 94.9, and the kappa was 0.85 ± 0.08, 95% CI: 0.81, 0.89. Including partial-thickness tears resulted in agreement of 65-92% and kappa values of 0.59-0.72. Conclusion: The reliability for the MRI detection of full thickness tears of the supraspinatus central tendon among shoulder surgeons and between shoulder surgeons and MSK radiologists was excellent. [Copyright &y& Elsevier]

Hypothesis: It is hypothesized that supraspinatus central tendon retraction is related to functional deficit; yet, there is no literature comparing the normal and pathological pennation and central tendon angles using magnetic resonance imaging (MRI). Therefore, the aim of this study was to quantify the anterior and posterior muscle pennation angles, central tendon angle, and retraction of the supraspinatus using MRI. Methods: Anterior pennation angle (APA), posterior pennation angle (PPA), and central tendon angle (CTA) were measured from 2 groups: no tear (NT, n = 157), full thickness tears (FTT) with retraction (FTT, n = 156). Results: No tear (NT) average APA, PPA, and CTA were 19.0° (SD 5.9), 4.0° (SD 3.2), and 17.8° (SD 5.1). All differences were statistically significant (PPA < APA, P < .001; PPA < CTA, P < .001; CTA < APA, P < .001). FTT averages were 17.6° (SD 8.6), 16.7° (SD 12.2), and 7.3° (SD 4.9). Increasing retraction correlated to PPA (P < .001), APA (P < .002), and CTA (P < .001). Conclusion: The size of a supraspinatus tear is directly correlated with muscle pennation and tendon retraction, and provides a direct measurement from MRI that can now be employed in further studies of functional deficit and tendon tear size. [ABSTRACT FROM AUTHOR]

Slit3 along with Slit1 and Slit2 comprise the Slit family of proteins. The latter two proteins are known to be involved in axon guidance and cell migration during animal development. However, little is know about the functions of Slit3. We created a Slit3-deficient mouse model from an OmniBank ES cell line with a Slit3 allele trapped by insertional mutagenesis to analyze the in vivo functions of this protein. In this model, congenital diaphragmatic hernia is the most obvious phenotype. Herniation was found to be caused by a defective central tendon (CT) of the diaphragm that remained fused with the liver. Electron microscopic analyses of the defective CT revealed disorganized collagen fibrils that failed to form tight collagen bundles. The hearts of Slit3-deficient mice have an enlarged right ventricle. In addition, 20% of homozygous mice also showed a range of kidney defects that include unilateral or bilateral agenesis of the kidney and ureter, or varying degrees of renal hypoplasia. Thus, we concluded that Slit3 is involved in the development of multiple organ systems that include the diaphragm and the kidney. Slit3-deficient mice represent a genetic animal model for physiological and pathological studies of congenital diaphragmatic hernia. [Copyright &y& Elsevier]