[Traumatic TFCC lesions in childhood and adolescence-A previously neglected injury?].

Although injuries to the triangular fibrocartilage complex (TFCC) are less common in children and adolescents than in adults, can lead to chronic pain and instability in the distal radioulnar joint (DRUJ), ultimately predisposing individuals to long-term osteoarthritis. A dislocated distal radius fracture with avulsion of the styloid process of the ulna following high-energy trauma is a risk factor for a TFCC injury. The diagnostics include a thorough clinical examination and imaging procedures, such as X‑ray and magnetic resonance imaging (MRI).

Non-fracture acute compartment syndrome in the upper extremity of a 14-year-old boy: A case report and review of the literature.

Introduction: Acute compartment syndrome (ACS) is an orthopaedic emergency affecting all age groups, yet diagnosis proves particularly difficult within the paediatric population and especially in the absence of fractures.

Case Presentation: In this case report, we detail a rare instance of a non-fracture acute compartment syndrome (NFACS) in a 14-year-old boy, initially missed due to lack of suspicion. Symptoms included swelling, severe pain, and initial paresthesia in the hand.

Missed Monteggia Injuries in Children and Adolescents: A Treatment Algorithm.

Monteggia injuries are rare childhood injuries. In 25-50% of cases, however, they continue to be overlooked, leading to a chronic Monteggia injury. Initially, the chronic Monteggia injury is only characterized by a moderate motion deficit, which is often masked by compensatory movements.

NovoSorb® Biodegradable Temporizing Matrix: a novel approach for treatment of extremity avulsion injuries in children.

Purpose: In pediatric population, large soft tissue defects occur in avulsion injuries. In addition to the challenges of primary surgical therapy, elasticity, appearance and function of the scar in children are of crucial importance, especially in the context of body growth. So far various flaps, plasties, skin grafts and dermal substitutes have become established, although infections and skin shrinkage remain challenging.

The paediatric polytrauma CT-indication (PePCI)-score-Development of a prognostic model to reduce unnecessary CT scans in paediatric trauma patients.

Background: Whole-Body CT (WBCT) is frequently used in emergency situations for promptly diagnosing paediatric polytrauma patients, given the challenges associated with obtaining precise details about the mechanism and progression of trauma. However, WBCT does not lead to reduced mortality in paediatric patients, but is associated with high radiation exposure. We therefore wanted to develop a screening tool for CT demand-driven emergency room (ER)-trauma diagnostic to reduce radiation exposure in paediatric patients.

Sharpin Controls Osteogenic Differentiation of Mesenchymal Bone Marrow Cells.

The cytosolic protein Sharpin is a component of the linear ubiquitin chain assembly complex, which regulates NF-κB signaling in response to specific ligands, such as TNF-α. Its inactivating mutation in chronic proliferative dermatitis mutation (Cpdm) mice causes multiorgan inflammation, yet this phenotype is not transferable into wild-type mice by hematopoietic stem cell transfer. Recent evidence demonstrated that Cpdm mice additionally display low bone mass, and that this osteopenia is corrected by Tnf deletion.

Impaired bone formation and increased osteoclastogenesis in mice lacking chemokine (C-C motif) ligand 5 (Ccl5).

Chemokines play crucial roles in the recruitment of specific hematopoietic cell types, and some of them have been suggested to be involved in the regulation of bone remodeling. Because we have previously observed that chemokine (C-C motif) ligand 2 (Ccl2) and Ccl5 are direct target genes of noncanonical Wnt signaling in osteoblasts, we analyzed the skeletal phenotypes of Ccl2-deficient and Ccl5-deficient mice. In line with previous studies, Ccl2-deficient mice display a moderate reduction of osteoclastogenesis at the age of 6 months.

Transgenic over-expression of interleukin-33 in osteoblasts results in decreased osteoclastogenesis.

Interleukin-33 (IL-33) is the most recently identified member of the IL-1 family of cytokines, which is primarily known for its proinflammatory functions. We have previously reported that IL-33 is expressed by bone-forming osteoblasts, and that administration of recombinant IL-33 to bone marrow cultures inhibits their differentiation into bone-resorbing osteoclasts. Likewise, while the inhibitory effect of IL-33 on osteoclast differentiation was fully abolished in cultures lacking the IL-33 receptor ST2, mice lacking ST2 displayed low bone mass caused by increased osteoclastogenesis.

Control of bone formation by the serpentine receptor Frizzled-9.

Although Wnt signaling in osteoblasts is of critical importance for the regulation of bone remodeling, it is not yet known which specific Wnt receptors of the Frizzled family are functionally relevant in this process. In this paper, we show that Fzd9 is induced upon osteoblast differentiation and that Fzd9(-/-) mice display low bone mass caused by impaired bone formation. Our analysis of Fzd9(-/-) primary osteoblasts demonstrated defects in matrix mineralization in spite of normal expression of established differentiation markers.

Interleukin-33 is expressed in differentiated osteoblasts and blocks osteoclast formation from bone marrow precursor cells.

Since the hematopoetic system is located within the bone marrow, it is not surprising that recent evidence has demonstrated the existence of molecular interactions between bone and immune cells. While interleukin 1 (IL-1) and IL-18, two cytokines of the IL-1 family, have been shown to regulate differentiation and activity of bone cells, the role of IL-33, another IL-1 family member, has not been addressed yet. Since we observed that the expression of IL-33 increases during osteoblast differentiation, we analyzed its possible influence on bone formation and observed that IL-33 did not affect matrix mineralization but enhanced the expression of Tnfsf11, the gene encoding RANKL.