Smith, Jay

Abstract Posterolateral rotatory instability (PLRI) is the most commonly encountered pattern of elbow instability. It is the result of disruption of the lateral collateral ligament complex leading to a posterolateral rotatory subluxation of the ulna and radial head. A number of examination maneuvers have been described to assist in clinical identification of PLRI. Despite this, some inconsistency in the description of these techniques remains in the orthopaedic literature. This Technical Note details the mechanism of injury and patient presentation, and emphasizes the primacy of the posterolateral rotatory drawer test in the assessment of PLRI while providing video instruction on how it should be performed. Technique Video video See video under supplementary data.

Abstract Currently, a number of examination and imaging techniques exist for diagnosing posterolateral rotatory instability of the elbow. Although the posterolateral rotatory drawer is the primary examination maneuver, other special tests include the lateral pivot‐shift test, prone push‐up test, chair push‐up test, and tabletop push‐up test. In addition, posterolateral rotatory instability can be evaluated using radiography, magnetic resonance imaging, dynamic fluoroscopy, or dynamic ultrasound. In this Technical Note, each of these tests is described in detail. Video instruction is also provided to further explain the techniques and provide examples of positive tests. Technique Video video See video under supplementary data.

Greater trochanteric pain syndrome is a common clinical entity that most often results from disorders of the gluteus medius tendon. There are two distinct bands of the gluteus medius tendon, and abnormalities may affect the anterior or posterior band in isolation or simultaneously. Although abnormalities of the anterior band are more common, awareness and sonographic detection of posterior band abnormalities is essential to guide treatment in the setting of greater trochanteric pain syndrome.

AbstractAdipose-derived mesenchymal stem cells (AMSCs) offer potential as a therapeutic option for clinical applications in musculoskeletal regenerative medicine because of their immunomodulatory functions and capacity for trilineage differentiation. In preparation for a phase I clinical trial using AMSCs to treat patients with osteoarthritis, we carried out preclinical studies to assess the safety of human AMSCs within the intra-articular joint space. Culture-expanded human AMSCs grown in human platelet-lysate were delivered via intra-articular injections into normal healthy rabbit knees and knees at risk for the development of osteoarthritis after bilateral medial anterior hemimeniscectomy. Treatment outcomes and safety were evaluated by assessing the general health, function, and behavior of the animals. Joint tissues were analyzed by x-ray, magnetic resonance imaging, and histopathology. Intra-articular AMSC therapy was well tolerated in this study. We did not observe adverse systemic reactions, nor did we find evidence of damage to intra-articular joint tissues. Thus, the data generated in this study show a favorable safety profile for AMSCs within the joint space in support of a phase I clinical trial evaluating the clinical utility of AMSCs to treat osteoarthritis.

Objective: To determine the optimal environmental conditions for chondrogenic differentiation of human adipose tissue–derived mesenchymal stromal/stem cells (AMSCs). In this investigation we specifically investigate the role of oxygen tension and 3-dimensional (3D) culture systems. Design: Both AMSCs and primary human chondrocytes were cultured for 21 days in chondrogenic media under normoxic (21% oxygen) or hypoxic (2% oxygen) conditions using 2 distinct 3D culture methods (high-density pellets and poly-ε-caprolactone [PCL] scaffolds). Histologic analysis of chondro-pellets and the expression of chondrocyte-related genes as measured by reverse transcriptase quantitative polymerase chain reaction were used to evaluate the efficiency of differentiation. Results: AMSCs are capable of expressing established cartilage markers including COL2A1, ACAN, and DCN when grown in chondrogenic differentiation media as determined by gene expression and histologic analysis of cartilage markers. Expression of several cartilage-related genes was enhanced by low oxygen tension, including ACAN and HAPLN1. The pellet culture environment also promoted the expression of hypoxia-inducible cartilage markers compared with cells grown on 3D scaffolds. Conclusions: Cell type–specific effects of low oxygen and 3D environments indicate that mesenchymal cell fate and differentiation potential is remarkably sensitive to oxygen. Genetic programming of AMSCs to a chondrocytic phenotype is effective under hypoxic conditions as evidenced by increased expression of cartilage-related biomarkers and biosynthesis of a glycosaminoglycan-positive matrix. Lower local oxygen levels within cartilage pellets may be a significant driver of chondrogenic differentiation.

ABSTRACTPreservation of osteochondral allografts used for transplantation is critical to ensure favorable outcomes for patients after surgical treatment of cartilage defects. To study the biological effects of protocols currently used for cartilage storage, we investigated differences in gene expression between stored allograft cartilage and fresh cartilage from living donors using high throughput molecular screening strategies. We applied next generation RNA sequencing (RNA‐seq) and real‐time reverse transcription quantitative polymerase chain reaction (RT‐qPCR) to assess genome‐wide differences in mRNA expression between stored allograft cartilage and fresh cartilage tissue from living donors. Gene ontology analysis was used to characterize biological pathways associated with differentially expressed genes. Our studies establish reduced levels of mRNAs encoding cartilage related extracellular matrix (ECM) proteins (i.e., COL1A1, COL2A1, COL10A1, ACAN, DCN, HAPLN1, TNC, and COMP) in stored cartilage. These changes occur concomitantly with increased expression of “early response genes” that encode transcription factors mediating stress/cytoprotective responses (i.e., EGR1, EGR2, EGR3, MYC, FOS, FOSB, FOSL1, FOSL2, JUN, JUNB, and JUND). The elevated expression of “early response genes” and reduced levels of ECM‐related mRNAs in stored cartilage allografts suggests that tissue viability may be maintained by a cytoprotective program that reduces cell metabolic activity. These findings have potential implications for future studies focused on quality assessment and clinical optimization of osteochondral allografts used for cartilage transplantation. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:1950–1959, 2016.

Snapping elbow is a well‐known condition where elbow flexion and extension elicits a painful, popping sensation. The most frequent etiology is anterior dislocation of the ulnar nerve over the medial epicondyle. Four patients (3 females and 1 male) presented with complaints of a popping sensation in the elbow, pain over the medial aspect of the forearm, and ulnar neuritis. All patients underwent preoperative dynamic ultrasound and surgical exploration of the medial elbow. Intraoperatively, snapping of the MABC over the medial epicondyle was discovered in all four patients. In three patients, there was abnormal displacement of the medial triceps and ulnar nerve: in two of these, both structures dislocated over the medial epicondyle and in one patient both structures subluxated. In each case, the MABC was decompressed (n = 1) and transposed (n = 3), and in three cases, the medial triceps and ulnar nerve were addressed as well. Symptomatic improvement was achieved in all cases. Retrospective review of the ultrasound revealed the snapping MABC, though it was less effective prospectively in the cases when snapping MABC was not suspected. In conclusion, snapping of the MABC broadens the spectrum of disorders that results in snapping elbow. To our knowledge, we are unaware of prior reports of this entity. Clin. Anat. 28:872–877, 2015. © 2015 Wiley Periodicals, Inc.