What Happens to Youth Baseball Players Diagnosed With Little League Shoulder and Little League Elbow Syndrome?

BACKGROUND: The long-term prognosis of baseball and softball players diagnosed with Little League elbow (LLE) and Little League shoulder (LLS) is unknown. Many of these athletes are potentially at risk of developing future shoulder and elbow injuries that may require surgical intervention. This study's purpose is to retrospectively assess 5-year patient-reported outcomes and career progression of a series of youth baseball and softball players diagnosed with LLE and LLS. METHODS: This institutional review board-approved, single-center, retrospective study evaluated 5-year outcomes of a cohort of youth baseball and softball players diagnosed with LLE and LLS between 2013 and 2017. Demographic and clinical data was recorded including age, gender, primary position, and months played per year. A standardized phone survey was obtained approximately 5 years post-treatment to assess upper extremity function, career progression, and pain recurrence. RESULTS: Sixty-one patients (44 LLE, 17 LLS) met the inclusion criteria and participated in a standardized phone survey. The mean age at the time of diagnosis was 13.2 years and all but one of the athletes were male. On average, about 80% (34/44 LLE, 15/17 LLS) played baseball 9 months or more per year. After diagnosis and nonoperative management, more than 80% (37/44 LLE, 14/17 LLS) were able to return to competition, but up to 40% of players changed positions (9/44 LLE, 7/17 LLS). Five years later, less than half (21/44 LLE, 8/17 LLS) were playing baseball actively. The recurrence rate was >20% (9/42 LLE, 6/17 LLS) with a mean time of recurrence of 8.8 months. Patients who experienced symptom recurrence were less likely to play baseball 5 years later and had lower patient-reported outcomes. CONCLUSIONS: A diagnosis of LLE and LLS in early adolescence can be a setback for a young athlete. Fortunately, most athletes will be able to return to competition with ∼50% still competing at 5 years. Very few will progress to future arm surgery, but recurrence rates are relatively high, and these athletes are less likely to participate in their sport 5 years later. LEVEL OF EVIDENCE: Level IV-Retrospective cohort study.

Skeletal Response to Soluble Activin Receptor Type IIB in Mouse Models of Osteogenesis Imperfecta.

Osteogenesis imperfecta (OI) is a heritable connective tissue disorder primarily due to mutations in the type I collagen genes (COL1A1 and COL1A2), leading to compromised biomechanical integrity in type I collagen-containing tissues such as bone. Bone is inherently mechanosensitive and thus responds and adapts to external stimuli, such as muscle mass and contractile strength, to alter its mass and shape. Myostatin, a member of the TGF-ß superfamily, signals through activin receptor type IIB to negatively regulate muscle fiber growth. Because of the positive impact of myostatin deficiency on bone mass, we utilized a soluble activin receptor type IIB-mFc (sActRIIB-mFc) fusion protein in two molecularly distinct OI mouse models (G610C and oim) and evaluated their bone properties. Wild-type (WT), +/G610C, and oim/oim mice were treated from 2 to 4 months of age with either vehicle (Tris-buffered saline) or sActRIIB-mFc (10 mg/kg). Femurs of sActRIIB-mFc-treated mice exhibited increased trabecular bone volume regardless of genotype, whereas the cortical bone microarchitecture and biomechanical strength were only improved in WT and +/G610C mice. Dynamic histomorphometric analyses suggest the improved cortical bone geometry and biomechanical integrity reflect an anabolic effect due to increased mineral apposition and bone formation rates, whereas static histomorphometric analyses supported sActRIIB-mFc treatment also having an anti-catabolic impact with decreased osteoclast number per bone surface on trabecular bone regardless of sex and genotype. Together, our data suggest that sActRIIB-mFc may provide a new therapeutic direction to improve both bone and muscle properties in OI. © 2018 American Society for Bone and Mineral Research.

Degeneration of the osteocyte network in the C57BL/6 mouse model of aging.

Age-related bone loss and associated fracture risk are major problems in musculoskeletal health. Osteocytes have emerged as key regulators of bone mass and as a therapeutic target for preventing bone loss. As aging is associated with changes in the osteocyte lacunocanalicular system, we focused on the responsible cellular mechanisms in osteocytes. Bone phenotypic analysis was performed in young-(5mo) and aged-(22mo) C57BL/6 mice and changes in bone structure/geometry correlated with alterations in osteocyte parameters determined using novel multiplexed-3D-confocal imaging techniques. Age-related bone changes analogous to those in humans were observed, including increased cortical diameter, decreased cortical thickness, reduced trabecular BV/TV and cortical porosities. This was associated with a dramatic reduction in osteocyte dendrite number and cell density, particularly in females, where osteocyte dendricity decreased linearly from 5, 12, 18 to 22mo and correlated significantly with cortical bone parameters. Reduced dendricity preceded decreased osteocyte number, suggesting dendrite loss may trigger loss of viability. Age-related degeneration of osteocyte networks may impair bone anabolic responses to loading and gender differences in osteocyte cell body and lacunar fluid volumes we observed in aged mice may lead to gender-related differences in mechanosensitivity. Therapies to preserve osteocyte dendricity and viability may be beneficial for bone health in aging.