Treatment trends of benign bone lesions in a suburban New York healthcare system.

Introduction: The management of benign bone lesions is controversial as it is dependent on a multitude of factors such as age, anatomic location, comorbidities, lesion metabolic activity, surgeon preferences, and goals of care, among others. Thus far, many studies have attempted to report on these lesions; however, most are heterogeneous compilations of benign and malignant lesions with nearly all failing to report patient treatment and none of which have originated from a suburban area of the United States. The goal of this study was to establish a modern database dedicated solely to benign bone tumors to reflect current diagnosis and treatment trends in suburban New York. Materials and Methods: This was a multicenter retrospective observational study with inclusion criteria limited to benign bone lesions of all ages. Malignant lesions were excluded. Patients were drawn from both primary care provider and surgeon records, with documentation of their associated management. Results: A total of 689 patients met inclusion criteria. The overall operative rate for this cohort was 71.6%. In agreement with current literature, aneurysmal bone cysts, giant cell tumors, and osteochondromas underwent surgery more frequently than enchondromas; older patients underwent surgery less frequently; benign bone lesions were more commonly found in younger males, and the distal femur and proximal tibia were the most common locations for lesions (P < .05 for all findings). Conclusion: This study demonstrates the management of a globally representative variety of benign bone lesions in a diverse suburban population of New York and should facilitate future research on how lesion type, location, management, and other factors relate to patient outcomes.

Activated CLL cells regulate IL-17F-producing Th17 cells in miR155-dependent and outcome-specific manners.

Chronic lymphocytic leukemia (CLL) results from expansion of a CD5+ B cell clone that requires interactions with other cell types, including T cells. Moreover, patients with CLL have elevated levels of circulating IL-17A+ and IL-17F+ CD4+ T (Th17) cells, with higher numbers of IL-17A+ Th17 cells correlating with better outcomes. We report that CLL Th17 cells expressed more miR155, a Th17-differentiation regulator, than control Th17 cells, despite naive CD4+ T (Tn) cell basal miR155 levels being similar in both. We also found that CLL cells directly regulated miR155 levels in Tn cells, thereby affecting Th17 differentiation, by documenting that coculturing Tn cells with resting or activated (Bact) CLL cells altered the magnitude and direction of T cell miR155 levels; CLL Bact cells promoted IL-17A+ and IL-17F+ T cell generation by an miR155-dependent mechanism, confirmed by miR155 inhibition; coculture of Tn cells with CLL Bact cells led to a linear correlation between the degree and direction of T cell miR155 expression changes and production of IL-17F but not IL-17A; and Bact cell-mediated changes in Tn cell miR155 expression correlated with outcome, irrespective of IGHV mutation status, a strong prognostic indicator. These results identify a potentially unrecognized CLL Bact cell-dependent mechanism, upregulation of Tn cell miR155 expression and subsequent enhancement of IL-17F+ Th17 generation, that favors better clinical courses.

Variability in Acetabular Component Position in Patients Undergoing Direct Anterior Approach Total Hip Arthroplasty Who Have Concomitant Spine Pathology.

BACKGROUND: Hip instability following total hip arthroplasty (THA) can be a major cause of revision surgery. Physiological patient position impacts acetabular anteversion and abduction, and influences the functional component positioning. Osteoarthritis of the spine leads to abnormal spinopelvic biomechanics and motion, but there is no consensus on the degree of component variability for THAs performed by anterior approach. Therefore, we sought to present guidelines for changes in acetabular component positioning between supine and standing positions for patients undergoing primary THA by a uniform anterior approach. METHODS: Perioperative patient radiographs of the pelvis and lumbar spine were collected. Images were used to determine acetabular component positioning and degree of coexisting spinal pathology, categorized as a Lane Grade (LG). Final analysis of variance was performed on a sample size of 643 anterior primary THAs. RESULTS: From supine to standing position, as the severity of lumbar pathology increased the change in anteversion also increased (LG:0 = -0.11° ± 4.65°, LG:1 = 2.02° ± 4.09°, LG:2-3 = 5.78° ± 5.72°, P < .001). The mean supine anteversion in patients with absent lumbar pathology was 19.72° ± 5.05° and was lower in patients with worsening lumbar pathology (LG:1 = 18.25° ± 4.81°, LG:2-3 = 16.73° ± 5.28°, P < .001). CONCLUSION: Patients undergoing primary THA by anterior approach with worsening spinal pathology have larger increases in component anteversion when transitioning from supine to standing positions. Consideration should be given to this expected variability when placing the patient's acetabular component.

Myeloid-derived suppressor cell subtypes differentially influence T-cell function, T-helper subset differentiation, and clinical course in CLL.

Cancer pathogenesis involves the interplay of tumor- and microenvironment-derived stimuli. Here we focused on the influence of an immunomodulatory cell type, myeloid-derived suppressor cells (MDSCs), and their lineage-related subtypes on autologous T lymphocytes. Although MDSCs as a group correlated with an immunosuppressive Th repertoire and worse clinical course, MDSC subtypes (polymorphonuclear, PMN-MDSC, and monocytic, M-MDSCs) were often functionally discordant. In vivo, PMN-MDSCs existed in higher numbers, correlated with different Th-subsets, and more strongly associated with poor clinical course than M-MDSCs. In vitro, PMN-MDSCs were more efficient at blocking T-cell growth and promoted Th17 differentiation. Conversely, in vitro M-MDSCs varied in their ability to suppress T-cell proliferation, due to the action of TNFα, and promoted a more immunostimulatory Th compartment. Ibrutinib therapy impacted MDSCs differentially as well, since after initiating therapy, PMN-MDSC numbers progressively declined, whereas M-MDSC numbers were unaffected, leading to a set of less immunosuppressive Th cells. Consistent with this, clinical improvement based on decreasing CLL-cell numbers correlated with the decrease in PMN-MDSCs. Collectively, the data support a balance between PMN-MDSC and M-MDSC numbers and function influencing CLL disease course.