Complex Lymphatic Anomalies (CLA) are lymphatic malformations with idiopathic bone and soft tissue involvement. The extent of the abnormal lymphatic presentation and boney invasion varies between subtypes of CLA. The etiology of these diseases has proven to be extremely elusive due to their rarity and irregular progression. In this review, we compiled literature on each of the four primary CLA subtypes and discuss their clinical presentation, lymphatic invasion, osseous profile, and regulatory pathways associated with abnormal bone loss caused by the lymphatic invasion. We highlight key proliferation and differentiation pathways shared between lymphatics and bone and how these systems may interact with each other to stimulate lymphangiogenesis and cause bone loss.

The aim of this review is to provide an updated review of the epigenetic factors involved in the onset and development of osteoarthritis (OA). OA is a prevalent degenerative joint disease characterized by chronic inflammation, ectopic bone formation within the joint, and physical and proteolytic cartilage degradation which result in chronic pain and loss of mobility. At present, no disease-modifying therapeutics exist for the prevention or treatment of the disease. Research has identified several OA risk factors including mechanical stressors, physical activity, obesity, traumatic joint injury, genetic predisposition, and age. Recently, there has been increased interest in identifying epigenetic factors involved in the pathogenesis of OA. In this review, we detail several of these epigenetic modifications with known functions in the onset and progression of the disease. We also review current therapeutics targeting aberrant epigenetic regulation as potential options for preventive or therapeutic treatment.

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Resiliency consists of three core components, which include presence of adversity, protective factors to overcome adversity, and positive outcomes or growth. Therefore, resiliency aligns with the trauma recovery process. This paper describes development of the Trauma Resiliency Scale (tRS) to quantify the resiliency of trauma patients upon presentation and during recovery. Scale items were proposed and reviewed by an expert panel. Group construct validity testing was performed using both individual and focus group feedback with item analysis. Reliability was measured with test–retest administered 14 days apart and evaluated with intraclass correlation coefficient. One hundred and twenty‐three items were initially proposed. Following item categorizing, a preliminary 17‐item questionnaire was created. The questionnaire was administered to 40 individual participants and a trauma survivor focus group to evaluate construct validity. Following group construct testing, an 18‐item Trauma Resiliency Scale (tRS‐18) was proposed. Twenty‐four participants were given the tRS‐18 twice, 14 days apart to establish test–retest. Sixteen of the 18 questions had an intraclass correlation >0.7 (0.793–0.949). The remaining two questions underperformed based on the ICC (0.592 and 0.493) and were manually evaluated for inclusion. The final tRS‐18 is a brief, self‐administered measure of resiliency designed specifically for trauma patients. Sound psychometric properties including face validity, construct validity, and reliability of the instrument have been demonstrated. The tRS‐18 may quantify resiliency at any time point with potential to be predictive of progress during recovery. Level of Evidence III, prognostic.