Nasoalveolar moulding for children with unilateral cleft lip and palate.

INTRODUCTION: Cleft lip and palate represents the most frequently occurring congenital deformity second only to club foot deformity in our country. Wide alveolar clefts if not preceded by pre surgical orthodontic adjuncts like nasoalveolar moulding, may affect the final outcome of the primary surgery. Presurgical nasoalveolar moulding is to align and approximate the alveolar cleft segments while at the same time achieving correction of the nasal cartilage and soft tissue deformity. MATERIALS AND METHODS: The device we used is designed by Barry Grayson. It is simple to fabricate, causes less discomfort to the patient and optimum results are achieved in three months of time, compared to other complicated appliances like Latham's which are more invasive. A child of 3 months presented with a complaint of unilateral cleft deformity on one side of the face. CONCLUSION: After three months of nasoalveolar moulding considerable changes were observed. The widths of the cleft alveolus were reduced and the nasal contours of columella on the cleft side showed considerable improvement.

Botox as an adjunct to orthognathic surgery for a case of severe vertical maxillary excess.

Large skeletal discrepancies are sometimes only minimised but not eliminated by orthognathic surgeries. Administration of Botox has been advocated as an effective minimally invasive procedure to tackle aesthetic compromises like gummy smile and the like. This article elaborates on the surgical management of a case of severe vertical maxillary excess with Botox as an adjunct therapy.

Pathogenomic mechanisms for particulate matter induction of acute lung injury and inflammation in mice.

To begin identifying genes controlling individual susceptibility to particulate matter, responses of inbred mouse strains exposed to nickel sulfate (NiSO4*) were compared with those of mice exposed to ozone (O3) or polytetrafluoroethylene (PTFE). The A strain was sensitive to NiSO4-induced lung injury (quantified by survival time), the C3H/He (C3) strain and several other strains were intermediate in their responses, and the C57BL/6 (B6) strain was resistant. The strains showed a pattern of response similar to the patterns of response to O3 and PTFE. The phenotype of A x B6 offspring (B6AF1) resembled that of the resistant B6 parental strain, with strains exhibiting sensitivity in the order A > C3 > B6 = B6AF1. Pathology was comparable for the A and B6 mice, and exposure to NiSO4 at 15 microg/m3 produced 20% mortality in A mice. Strain sensitivity for the presence of protein or neutrophils in lavage fluid differed from strain sensitivity for survival time, suggesting that they are not causally linked but are controlled by an independent gene or genes. In the B6 strain, exposure to nickel oxide (NiO) by instillation (40 to 1000 nm) or inhalation (50 nm) produced no changes, whereas inhalation of NiSO4 (60 or 250 nm) increased lavage proteins and neutrophils. Complementary DNA (cDNA) microarray analysis with 8,734 sequence-verified clones revealed a temporal pattern of increased oxidative stress, extracellular matrix repair, cell proliferation, and hypoxia, followed by a decrease in surfactant-associated proteins (SPs). Certain expressed sequence tags (ESTs), clustered with known genes, suggest possible coregulation and novel roles in pulmonary injury. Finally, locus number estimation (Wright equation) and a genomewide analysis suggested 5 genes could explain the survival time and identified significant linkage for a quantitative trait locus (QTL) on chromosome 6, Aliq4 (acute lung injury QTL4). Haplotype analysis identified an allelic combination of 5 QTLs that could explain the difference in sensitivity to acute lung injury between parental strains. Positional candidate genes for Aliq4 include aquaporin-1 (Aqp1), SP-B, and transforming growth factor-alpha (TGF-alpha). Transgenic mice expressing TGF-alpha were rescued from NiSO4 injury (that is, they had diminished SP-B loss and increased survival time). These findings suggest that NiSO4-induced acute lung injury is a complex trait controlled by at least 5 genes (all possibly involved in cell proliferation and surfactant function). Future assessment of these susceptibility genes (including evaluations of human synteny and function) could provide valuable insights into individual susceptibility to the adverse effects of particulate matter.