Root and Eruption Defects in c-Fos Mice Are Driven by Loss of Osteoclasts.

c-Fos homozygous mice lack osteoclasts with a failure of the teeth to erupt and with an arrest of root development. Here, we characterize the defects associated with the failure in root development and the loss of the tooth-bone interface, and we investigate the underlying causes. We show that, while homozygous c-Fos mice have no multinucleated osteoclasts, heterozygous mice have a reduction in the number of osteoclasts with a reduction in the tooth-bone interface during development and subtle skeletal defects postnatally. In the homozygous mutants bone is found to penetrate the tooth, particularly at the apical end, physically disrupting the root forming HERS (Hertwig's epithelial root sheath) cells. The cells of the HERS continue to proliferate but cannot extend downward due to the presence of bone, leading to a loss of root formation. Tooth germ culture showed that the developing tooth invaded the static bone in mutant tissue, rather than the bone encroaching on the tooth. Although c-Fos has been shown to be expressed in developing teeth, the defect in maintenance of the tooth-bone interface appears to be driven solely by the lack of osteoclasts, as this defect can be rescued in the presence of donor osteoclasts. The rescue suggests that signals from the tooth recruit osteoclasts to clear the bone from around the tooth, allowing the tooth to grow, form roots, and later erupt.

Antibacterial activity of peptides homologous to a loop region in human lactoferrin.

Human lactoferrin contains a 46 residue sequence named lactoferricin H thought to be responsible for its antimicrobial properties. Synthetic peptides HLT1, corresponding to the loop region of human lactoferricin (FQWQR-NMRKVRGPPVS) and HLT2, corresponding to its charged portion (FQWQRNMRKVR), exerted significant antibacterial effects against E. coli serotype O111 strains NCTC 8007 and ML35. The corresponding sequences in native human lactoferrin were shown to adopt a charged helix and hydrophobic tail within the N-lobe remote from the iron binding site. Sequence similarities between lactoferricin and dermaseptin and magainins suggest that lactoferricin may act as an amphipathic alpha helix.

Dynamization timing and its effect on bone healing when using the Orthofix Dynamic Axial Fixator.

We report the effect of dynamization timing on healing rates when treating tibial fractures with the Dynamic Axial Factor (Orthofix, registered trademark). Sixty-nine patients with 71 fresh tibial fractures were grouped retrospectively for age, Gustilo and Anderson wound grading, site of tibial fracture and presence of an intact fibula or stable fibular fracture. Pairs were then generated chronologically to compare healing rates in those patients dynamized before 4 weeks with those dynamized after this time. This resulted in 22 pairs of patients; the other fractures could not be paired. Their healing times were compared using a paired t-test and were found to be significantly quicker in the group dynamized within the first 4 weeks (P < 0.05) and we therefore recommend that this should be routine practice.