Early Tooth Loss in Children: A Warning Sign of Childhood Hypophosphatasia.

Premature exfoliation of primary teeth may be the first manifestation of this serious condition and the general dental practitioner plays an important role in recognizing dental anomalies and referring patients at an appropriate time. This is imperative to ensuring early diagnosis and good quality patient care. This article describes the case of a 4-year-old boy affected by childhood hypophosphatasia, who presented with premature exfoliation of his primary teeth as the first manifestation of this condition. An overview of the condition is outlined including a discussion of the likelihood of permanent dentition involvement. Clinical relevance: Oral manifestations of hypophosphatasia may be the first and the only signs of this condition and may be the basis upon which a diagnosis is made.

Mutations in Turnip mosaic virus P3 and cylindrical inclusion proteins are separately required to overcome two Brassica napus resistance genes.

The Brassica napus differential line 165 is resistant to infection by Turnip mosaic virus (TuMV) isolates belonging to pathotypes 1 and 3. Nucleotide sequences of resistance-breaking mutants of pathotype 1 (UK 1), pathotype 3 (CHN 12), and wild-type isolates have been determined. When the mutations identified were introduced into an infectious clone of UK 1, a single mutation in the viral P3 protein induced a hypersensitive (necrotic) response in inoculated leaves of line 165 plants. Full systemic nonnecrotic infection was only possible when another mutation (in the cylindrical inclusion protein) was introduced. Tests on segregating populations derived from line 165 indicated that the two viral genes were pathogenicity determinants for two different resistance genes in line 165. One gene responsible for an extreme form of resistance (no symptoms seen) was epistatic to a second responsible for the hypersensitive reaction. These results help to explain the relative stability of the resistance in line 165 and to further define the genetic basis of the TuMV pathotyping system.