Abstract
INTRODUCTION. Periodontal disease and permanent tooth loss are rampant worldwide. Periostin, a “matricellular” protein within the periodontal ligament (PDL) of humans and mice, conveys change in mechanical loading to influence cell function, cell-matrix interactions, and periodontal tissue homeostasis. Unlike humans, mice have continually growing incisors. We hypothesized that growing incisor sheer stress and molar occlusal force mandate differential expression of Periostin isoforms to account for functional differences in cell-matrix communication in the PDL of these unique tooth domains. METHODS. Using a model of human periodontal disease, we evaluated dental tissue and alveolar bone changes in Postntm1Jmol homozygous mice using micro-CT scanning, photo-radiography and histology. Using reverse transcriptase and the polymerase chain reaction (RT-PCR), differential expression of Periostin isoforms in wild-type soft tissue surrounding the molar and incisor teeth was assessed. SUMMARY. Anatomical evaluation of mandibles from 3 week old and 4-7 month-old Periostin mutant and wild-type mice revealed a space between the molars and the underlying incisor (n=4, U=0) in only the 4-7 month old homozygous mutant mice. RT-PCR showed that the mouse (C57Bl/6J) only expresses a single isoform lacking 2 exons (ΔbΔe), unlike the 5 isoforms expressed in human PDL. CONCLUSIONS. We quantified an increase in the distance between mandibular molars and the underlying incisor in Postntm1Jmol homozygous mutants. This is most likely the result of a functional/structural degradation of the periodontium and supporting bone suggesting a functional niche for Periostin exists, that is distinct from that found in the PDL. While we expected to find multiple PDL isoforms of Periostin that would correlate with functionally unique PDLs, our evidence suggests that only one isoform (ΔbΔe) of Periostin exists in adult mouse PDL.