Rats treated with AZD2858, a GSK3 inhibitor, heal fractures rapidly without endochondral bone formation.

Fracture healing is a complex interplay between endochondral and intramembranous bone formation processes. The canonical Wnt/β-catenin pathway enhances new bone formation and may play a role in fracture healing. Glycogen synthase kinase 3β (GSK3β) is a key regulator of β-catenin degradation.

GSK-3 inhibition by an orally active small molecule increases bone mass in rats.

Glycogen synthase kinase 3β (GSK-3β) actions are central in the canonical Wnt pathway, important in many biological processes and a potential drug target for treating several diseases. It is appreciated that a balanced Wnt canonical signaling is crucial for the maintenance of normal bone mass. In this study we investigated the effects of a potent orally active GSK-3 inhibitor, AZD2858, on bone mass in rats.

Bone formation in interleukin-4 and interleukin-13 depleted mice.

Background And Purpose: Cytokines play an important role in the complex process of bone formation. We have previously found an altered skeletal phenotype with reduction of cortical bone mass in mice depleted of the 2 cytokines interleukin-4 (IL-4) and interleukin-13 (IL 13). The present study was performed to investigate a potential role of IL-4 and IL-13 in fracture healing and bone induction by demineralized xenogenic bone matrix (DXBM).

Neutrophil CD64 (FcgammaRI) expression is a specific marker of bacterial infection: a study on the kinetics and the impact of major surgery.

Neutrophil CD64 expression is a diagnostic marker for the early detection of bacterial infections. The aim was to investigate the kinetics of neutrophil CD64 expression during bacterial infection and the possible impact of surgical trauma. Blood samples were collected daily during 3 d after admission for analysis by flow cytometry of the surface expressions on neutrophils and monocytes of CD64, CD16, CD32, CD11b/CD18 and CD35, and analysis of serum CRP and blood WBC.

Indomethacin inhibits bone formation in inductive allografts but not in autografts: studies in rat.

Background: Non-steroidal anti-inflammatory drugs (NSAIDs) are known to have inhibitory effects on new bone formation. We wanted to analyze some effects of the NSAID indomethacin on different inductive stimuli for bone formation.

Methods: We experimentally induced heterotopic new bone with demineralized allogeneic bone matrix (DABM) and with bone autografts in rats, in order to study the effects of indomethacin on new bone formation at 3 and 6 weeks.